A9-Evolution-Fact-Theory.txt

Graham L. Kendall
Modified  6/26/2002
http://www.grahamkendall.net/ 
Email grahamkendall74135@yahoo.com
I am found on IRC Efnet/Undernet/Dalnet as glk

Author: Larry A. Moran (lamoran@gpu.utcs.utoronto.ca)  
 Title: Evolution is a Fact and a Theory  
============================================================================  
                    EVOLUTION AS A FACT AND A THEORY  
                     version 2.1 (January 22, 1993)  
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When non-biologists talk about biological evolution they often confuse two   
different aspects of the definition. On the one hand there is the question   
of whether or not modern organisms have evolved from older ancestral organisms
or whether modern species are continuing to change over time. On the 
other hand there are questions about the mechanism of the observed changes...
how did evolution occur? Biologists consider the existence of 
biological evolution to be a FACT. It can be demonstrated today and the
historical evidence for it's occurrence in the past is overwhelming. However,

biologists readily admit that they are less certain of the exact MECHANISM of
evolution; there are several THEORIES of the mechanism of evolution. 
 
Stephan J. Gould has put this as well as anyone else, 

"In the American vernacular, "theory" often means "imperfect fact" 
- part of a hierarchy of confidence running downhill from fact to 
theory to hypothesis to guess. Thus the power of the creationist  
argument: evolution is "only" a theory and intense debate now rages  
about many aspects of the theory. If evolution is worse than a fact, 
and scientists can't even make up their minds about the theory, then 
what confidence can we have in it? Indeed, President Reagan echoed 
this argument before an evangelical group in Dallas when he said  
(in what I devoutly hope was campaign rhetoric): 'Well, it is a  
theory. It is a scientific theory only, and it has in recent years 
been challenged in the world of science - that is, not believed in 
the scientific community to be as infallible as it once was.' 
Well evolution is a theory. It is also a fact. And facts and theories 
are different things, not rungs in a hierarchy of increasing certainty.
Facts are the world's data. Theories are structures of ideas that 
explain and interpret facts. Facts don't go away when scientists 
debate rival theories to explain them. Einstein's theory of gravitation
replaced Newton's in this century, but apples didn't suspend
themselves in midair, pending the outcome. And humans evolved from
ape-like ancestors whether they did so by Darwin's proposed mechanism or by
some other yet to be discovered. Moreover, 'fact' doesn't mean 'absolute
certainty'; there ain't no such animal in an exciting and complex world.
The final proofs of logic and mathematics flow deductively from stated premises
and achieve certainty only because they are NOT about the empirical 
world. Evolutionists make no claim for perpetual truth, though 
creationists often do (and then attack us falsely for a style of 
argument that they themselves favor). In science 'fact' can only 
mean 'confirmed to such a degree that it would be perverse to 
withhold provisional consent'. I suppose that apples might start 
to rise tomorrow, but the possibility does not merit equal time in 
physics classrooms. 

      Evolutionists have been very clear about this distinction of fact 
      and theory from the very beginning, if only because we have always 
      acknowledged how far we are from completely understanding the 
      mechanisms (theory) by which evolution (fact) occurred. Darwin 
      continually emphasized the difference between his two great and 
      separate accomplishments: establishing the fact of evolution, and 
      proposing a theory - natural selection - to explain the mechanism 
      of evolution." 
      Stephen J. Gould "Evolution as Fact and Theory"; Discover, May 1981 

Gould is stating the prevailing view of the scientific community. In other  
words, the experts on evolution consider it to be a FACT.
This is not an idea that originated with Gould as the following quotations
indicate; 

"Let me try to make crystal clear what is established beyond  
reasonable doubt, and what needs further study, about evolution. 
Evolution as a process that has always gone on in the history of 
the earth can be doubted only by those who are ignorant of the  
evidence or are resistant to evidence, owing to emotional blocks 
or to plain bigotry. By contrast, the mechanisms that bring  
evolution about certainly need study and clarification. There are 
no alterantives to evolution as history that can withstand critical 
examination. Yet we are constantly learning new and important facts 
about evolutionary mechanisms." 

      Theodosius Dobzhansky "Nothing in Biology Makes Sense Except in the 

      Light of Evolution", American Biology Teacher vol.35 (March 1973) 

      reprinted in EVOLUTION VERSUS CREATIONISM, J. Peter Zetterberg ed.,

      ORYX Press, Phoenix AZ 1983 

     "It is time for students of the evolutionary process, especially  
      those who have been misquoted and used by the creationists, to  
      state clearly that evolution is a FACT, not theory, and that what 
      is at issue within biology are questions of details of the process 
      and the relative importance of different mechanisms of evolution. 
      It is a FACT that the earth with liquid water, is more than 3.6 
      billion years old. It is a FACT that cellular life has been around  
      for at least half of that period and that organized multicellular 
      life is at least 800 million years old. It is a FACT that major  
      life forms now on earth were not at all represented in the past.  
      There were no birds or mammals 250 million years ago. It is a FACT 
      that major life forms of the past are no longer living. There used 
      to be dinosaurs and Pithecanthropus, and there are none now. It is 
      a FACT that all living forms come from previous living forms.  
      Therefore, all present forms of life arose from ancestral forms that 
      were different. Birds arose from nonbirds and humans from nonhumans. 
      No person who pretends to any understanding of the natural world 
      can deny these facts any more than she or he can deny that the  
      earth is round, rotates on its axis, and revolves around the sun. 
           The controversies about evolution lie in the realm of the 
      relative importance of various forces in molding evolution." 
      R. C. Lewontin "Evolution/Creation Debate: A Time for Truth" 
      Bioscience 31, 559 (1981) reprinted in EVOLUTION VERSUS CREATIONISM 
      op cit. 

This concept is also explained in introductory biology books that are used in
colleges and universities (and in some of the better high schools). For
example, in some of the best such textbooks we find, 

     "Today, nearly all biologists acknowledge that evolution is a fact. 
      The term THEORY is no longer appropriate except when referring to 
      the various models that attempt to explain HOW life evolves... 
      it is important to understand that the current questions about 
      how life evolves in no way implies any disagreement over the fact 
      of evolution." 
      Neil A. Campbell, BIOLOGY 2nd ed., 1990, Benjamin/Cummings, p.434 

     "Since Darwin's time, massive additional evidence has accumulated 
      supporting the fact of evolution - that all living organisms present 
      on earth today have arisen from earlier forms in the course of 
      earth's long history. Indeed, all of modern biology is an affirmation 
      of this relatedness of the many species of living things and of 
      their gradual divergence from one another over the course of time. 
      Since the publication of The Origin of Species, the important  
      question, scientifically speaking, about evolution has not been 
      whether it has taken place. That is no longer an issue among the  
      vast majority of modern biologists. Today, the central and still 
      fascinating questions for biologists concern the mechanisms by 
      which evolution occurs." 

      Helena Curtis and N. Sue Barnes, BIOLOGY 5th ed. 1989, 
      Worth Publishers, p.972 

One of the best introductory books on evolution (as opposed to introductory 
biology) is that by Douglas J. Futuyma, and he makes the following comment, 

     "A few words need to be said about the 'theory of evolution', which 
      most people take to mean the proposition that organisms have evolved 
      from common ancestors. In everyday speech, 'theory' often means a 
      hypothesis or even a mere speculation. But in science, 'theory' 
      means 'a statement of what are held to be the general laws, principles,
      or causes of something known or observed", as the Oxford English 
      Dictionary defines it. The theory of evolution is a body of  
      interconnected statements about natural selection and the other  
      processes that are thought to cause evolution, just as the atomic 
      theory of chemistry and the Newtonian theory of mechanics are bodies 
      of statements that describe causes of chemical and physical phenomena
      In constrast, the statement that organisms have descended with  
      modifications from common ancestors - the historical reality of 
      evolution - is not a theory. It is a fact, as fully as the fact of 
      the earth's revolution about the sun. Like the heliocentric solar 
      system, evolution began as a hypothesis, and achieved "facthood" as 
      the evidence in its favor became so strong that no knowledgeable 
      and unbiased person could deny its reality. No biologist today 
      would think of submitting a paper entitled "New evidence for  
      evolution"; it simply has not been an issue for a century." 

Douglas J. Futuyma, op. cit., p.15 

There are readers of these newsgroups who reject evolution for religious  
reasons. In general these readers oppose both the FACT of evolution and  
THEORIES of mechanisms although some anti-evolutionists have come to realize 
that there is a difference between the two concepts. That is why we see
some  leading anti-evolutionists admitting to the fact of "microevolution" -
they  know that evolution can be demonstrated. These readers will not be
convinced of the "facthood" of (macro)evolution by any logical argument and it
is a  
waste of time to make the attempt. The best that we can hope for is that
they understand the argument that they oppose. Even this simple hope is
rarely fulfilled. 

There are some readers who are not anti-evolutionist but still claim that  
evolution is "only" a theory which can't be proven. This group needs to  
distinguish between the fact that evolution occurs and the theory of the  
mechanism of evolution. 

We also need to distinguish between facts that are easy to demonstrate and 
those that are more circumstantial. Examples of evolution that are readily 
apparent include the fact that modern populations are evolving and the fact 
that two closely related species share a common ancestor. The evidence that 
Homo sapiens and chimpanzees share a recent common ancestor falls into this 
catagory. There is so much evidence in support of this aspect of primate 
evolution that it qualifies as a fact by any common definition of the word 
"fact". 

In other cases the available evidence is less strong. For example, the  
relationships of some of the major phyla are still being worked out. Also, 
the statement that all organisms have descended from a single common ancestor
is strongly supported by the available evidence, and there is no opposing 
evidence. However, it is not yet appropriate to call this a "fact" since
there are reasonable alternatives. 

Finally, there is an epistemological argument against evolution as fact.
Some readers of these newsgroups point out that nothing in science can
ever be "proven" and this includes evolution. According to this argument,
the probability that evolution is the correct explanation of life as we
know it may approach 99.9999...9% but it will never be 100%. Thus evolution
cannot be a fact. This kind of argument might be appropriate in a philosophy
class (it is essentially correct) but it won't do in the real world. A
"fact", as Stephen J. Gould pointed out (see above), means something
that is so highly probable that it would be silly not to accept it. This point
has also been made by others who contest the nit-picking epistemologists. 

 "The honest scientist, like the philosopher, will tell you that 
nothing whatever can be or has been proved with fully 100% 
certainty, not even that you or I exist, nor anyone except himself, 
since he might be dreaming the whole thing. Thus there is no sharp  
line between speculation, hypothesis, theory, principle, and fact, 
but only a difference along a sliding scale, in the degree of 
probability of the idea. When we say a thing is a fact, then, we 
only mean that its probability is an extremely high one: so high 
that we are not bothered by doubt about it and are ready to act  
accordingly. Now in this use of the term fact, the only proper one, 
evolution is a fact. For the evidence in favor of it is as voluminous, 
diverse, and convincing as in the case of any other well
established fact of science concerning the existence of things that cannot be 
directly seen, such as atoms, neutrons, or solar gravitation .... 
So enormous, ramifying, and consistant has the evidence for 
evolution become that if anyone could now disprove it, I should 
have my conception of the orderliness of the universe so shaken  
as to lead me to doubt even my own existence. If you like, then, 
I will grant you that in an absolute sense evolution is not a fact, 
or rather, that it is no more a fact than that you are hearing or 
reading these words." 
H. J. Muller, "One Hundred Years Without Darwin Are Enough" 
School Science and Mathematics 59, 304-305. (1959) reprinted 
in EVOLUTION VERSUS CREATIONISM op cit. 

In any meaningful sense evolution is a fact but there are various theories 
concerning the mechanism of evolution. 
Laurence A. Moran (Larry) 
======================================================================

Author: Chris Colby (colby@bu-bio.bu.edu)

 Title: FAQ: Introduction to Evolutionary Biology

======================================================================
AN INTRODUCTION TO EVOLUTIONARY BIOLOGY -- BY CHRIS COLBY
*********************************************************
INTRODUCTION

Evolution is one of the most powerful theories science has ever 
known. For a variety of reasons, however, it is also one of the 
most misunderstood. One common misunderstanding is that the 
phrase "survival of the fittest" summarizes evolutionary theory. It 
does not. The phrase is both incomplete and misleading. Two other 
common misinterpretations are that evolution is progress and 
organisms can be arranged on an evolutionary ladder from bacteria 
to man. 
This post is an outline of the basics of evolutionary biology. It is 
intended to be an overview of the concepts and mechanisms of 
evolution and dispel pervasive misunderstandings about the theory. 
Creationist arguments are not addressed here; and many 
interesting topics in evolutionary biology are not covered 
(symbiosis and endosymbiosis, origins of life, evolution of sex, 
human evolution and much more) because I can't include everything 
and keep this down to a readable length. 

WHAT IS EVOLUTION?

Evolution is a change in the gene pool of a population over time. 
The gene pool is the set of all genes in a species or population. The 
English moth, _Biston__betularia_, is a frequently cited example 
of observed evolution. In this moth, rare black variants spread 
through the population as a result of their habitat becoming 
darkened by soot from factories. Birds could see the lighter 
colored moths more readily and ate more of them. The moth 
population changed from mostly light colored moths to mostly dark 
colored moths. Since their color was determined by a single gene, 
the change in frequency of dark colored moths represented a 
change in the gene pool. This change was, by definition, evolution. 

The kind of evolution documented above is called "microevolution". 
Larger changes (taking more time) are termed "macroevolution". 
Some biologists feel the mechanisms of macroevolution are 
different from those of microevolutionary change. Others, 
including myself, feel the distinction between the two is 
arbitrary. Macroevolution is cumulative microevolution.

In any case, evolution is defined as a change in the gene pool. This 
means that evolution is a population level phenomena. Only groups 
of organisms evolve. An individual organism does not evolve, nor 
do subunits of organisms evolve (with limited exceptions). So, 
when thinking of evolution, is necessary to view populations as a 
collection of individuals with different traits. For example, in the 
example above the frequency of black moths increased, the 
"average" moth did not get progressively darker. Indeed there were 
no "average" half-white/half-black moths ever in the population.

I have defined evolution, here, as a process and that is how I will 
use the term in this essay. Keep in mind, however, that in everyday 
use evolution refers to a variety of things. The fact that all 
organisms are linked via descent to a common ancestor is often 
called evolution. The theory that life arose solely via natural 
processes is often called evolution (instead of abiogenesis). And 
frequently, people use the word evolution when they really mean 
natural selection -- one of the many mechanisms of evolution. 

WHAT ISN'T EVOLUTION? 

For many, evolution is equated with morphological change, i.e. 
organisms changing shape or size over time. An example would be a 
dinosaur species evolving into a species of bird. It is important to 
note that evolution is often accompanied by morphological change, 
but this need not be the case. Evolution can occur without 
morphological change; and morphological change can occur without 
evolution. For instance, humans are larger now than in the past, 
but this is not an evolutionary change. Better diet and medicine 
brought about this change, so it is not an example of evolution. The 
gene pool did not change -- only its manifestation did.
An organism's phenotype is determined by its genes and its 
environment. Phenotype is the morphological, physiological, 
biochemical, behavioral and other properties exhibited by a living 
organism. Phenotypic changes induced solely by changes in 
environment do not count as evolution because they are not 
heritable; in other words the change is not passed on to the 
organism's offspring. Most changes due to environment are fairly 
subtle (e.g. size differences). Large scale phenotypic changes (such 
as dinosaur to bird) are obviously due to genetic changes, and 
therefore are evolution. 

WHAT EVOLUTION ISN'T 

Evolution is not progress. Organisms simply adapt to their current 
surroundings and do not necessarily become "better" over time. A 
trait or strategy that is successful at one time may be deleterious 
at another. Studies in yeast have shown that "more evolved" 
strains of yeast can be competitively inferior to "less evolved" 
strains. An organism's success depends a great deal on the 
behavior of its contemporaries; for most traits or behaviors there 
is likely no optimal design or strategy, only contingent ones. 

HOW DOES EVOLUTION WORK? 

If evolution is a change in the gene pool; what causes the gene pool 
to change? Several mechanisms can change a gene pool, among 
them: natural selection, genetic drift, gene flow, mutation and 
recombination. I will discuss these in more detail later. It is 
important to understand the difference between evolution and the 
mechanisms that bring about this change. 

GENETIC VARIATION

Bringing about a change in the gene pool assumes that there is 
genetic variation in the population to begin with, or a way to 
generate it. Genetic variation is "grist for the evolutionary mill". 
For example, if there were no dark moths, the population could not 
have evolved from mostly light to mostly dark. In order for 
continuing evolution there must be mechanisms to increase or 
create genetic variation (e.g. mutation) and mechanisms to 
decrease it (e.g. natural selection and genetic drift). 

HOW IS GENETIC VARIATION DESCRIBED? 

Genetic variation has two components: allelic diversity and non-
random associations of alleles. Alleles are different versions of 
the same gene at a given locus (locus means location). For 
example, at the blood group locus  humans can have an A, B or O 
allele. Most animals, including humans, are diploid. This means 
they contain two alleles for every gene at every locus. If the two 
alleles are the same type (for instance two A alleles) the 
individual would be termed "homozygous" for that locus. An 
individual with two different alleles at a locus is called 
"heterozygous". Allelic diversity is simply the number of alleles 
at each locus scaled by their frequency in the gene pool. At any 
locus there can be many different alleles, more alleles than any 
single organism can possess. 

Linkage disequilibrium is a measure of association between 
alleles at different loci. If each gene assorted entirely 
independently, the gene pool would be at linkage equilibrium. 
However, if some alleles were often found together in organisms 
(i.e. did not assort randomly) these alleles would be in linkage 
disequilibrium. Linkage disequilibrium can be the result of 
physical proximity of the genes or maintained by natural selection 
if some combinations of alleles work better as a team. 

HOW MUCH GENETIC VARIATION IS THERE? 

Considerable variation has been detected in natural populations. At 
45 percent of loci in plants there is more than one allele in the 
gene pool. Any given plant is likely to be heterozygous at about 15 
percent of its loci. Levels of genetic variation in animals range 
from roughly 15% of loci having more than one allele (polymorphic) 
in birds, to over 50% of loci being polymorphic in insects. 
Mammals and reptiles are polymorphic at about 20% of their loci - 
- amphibians and fish are polymorphic at around 30% of their loci. 
Most loci assort independently (i.e. they are at linkage 
equilibrium). In most populations, there are enough loci and enough 
different alleles that every individual (barring monozygotic 
(identical) twins) has a unique combination of alleles. 

EVOLUTION WITHIN A LINEAGE (ANAGENESIS)

The following sections deal with evolution within a population or 
lineage -- this is called anagenesis. Several mechanisms can bring 
about anagenetic change. I have grouped them into two classes -- 
those that decrease genetic variation and those that increase it. 

MECHANISMS THAT DECREASE GENETIC VARIATION 

------------------------------------------ 

MECHANISMS OF EVOLUTION: NATURAL SELECTION 

Natural selection is the only mechanism of adaptive evolution; it 
is defined as differential reproductive success of pre-existing 
classes of genetic variants in the gene pool. In other words, some 
genotypes are (on average) better than others at contributing their 
alleles to the next generation's gene pool. 

Selection is not a force in the sense that gravity or magnetism is. 
However, biologists often, for the sake of brevity, refer to it that 
way. Selection is not a guided or cognizant entity; it is simply an 
effect. 

When supplied with genetic variation, natural selection allows 
organisms to adapt to their current environment. It does not, 
however, have any foresight. Structures or behaviors do not evolve 
for future utility. An organism must be, to some degree, adapted to 
its environment at each stage of its evolution. As the environment 
changes, new traits (new combinations of alleles) may be selected 
for.  Large changes in populations are the result of cumulative 
natural selection -- numerous small changes are introduced into 
the population by mutation; the small minority of these changes 
that result in a greater reproductive output of their bearers are 
amplified in frequency by selection.
If evolution proceeds without any foresight, it is logical to wonder 
how complex traits evolve? If half a wing is no good for flying, 
how did wings evolve? Half a wing may be no good for flying, but it 
may be useful in other ways. Feathers are thought to have evolved 
as insulation (ever worn a down jacket?) and/or as a way to trap 
insects. Later, proto-birds may have learned to glide when leaping 
from tree to tree. Eventually, the feathers that originally served 
as insulation now became co-opted for use in flight. 

This illustrates the point that a trait's current utility is not 
always indicative of its past utility. It can evolve for one purpose, 
and be used later for another. A trait evolved for its current 
utility is an adaptation; one that evolved for another utility is an 
exaptation. An example of an exaptation is a penguin's wing. 
Penguins evolved from flying ancestors; now they are flightless 
and use their wings for swimming. 

Natural selection works at the level of the individual. The example 
I gave earlier was an example of evolution via natural selection. 
Dark colored moths had higher reproductive success because light 
colored moths suffered a higher predation rate. The decline of 
light colored alleles was caused by light colored individuals being 
removed from the gene pool (selected against). It is the individual 
organism that either reproduces or fails to reproduce. Genes are 
not the unit of selection (because their success depends on the 
organism's other genes as well); neither are groups of organisms a 
unit of selection. There are some exceptions to this "rule". 

The individual organism reproduces or fails to reproduce. It 
competes primarily with others of it own species for its 
reproductive success. For this reason organisms do not perform 
any behaviors that are for the good of their species. Natural 
selection favors selfish behavior because any truly altruistic act 
increases the recipient's reproductive success while lowering the 
donors. Altruists would quickly disappear from a population as the 
non-altruists would reap the benefits, but not pay the cost, of any 
altruistic act.

Of course, many behaviors appear to be altruistic. Biologists, 
however, can demonstrate (in the cases they have studied) that 
these behaviors are only apparently altruistic. Cooperating with or 
helping other organisms is often the most selfish strategy for an 
animal. Often this is called "reciprocal altruism" (an oxymoron if 
there ever was one). A good example of this is blood sharing in 
vampire bats. In these bats, those lucky enough to find a meal will 
often share part of it with an unsuccessful bat by regurgitating 
some blood into the other's mouth. Biologists have found that these 
bats form bonds with partners and help each other out when the 
other is needy. If a bat is found to be a "cheater", (i.e. he accepts 
blood when starving, but does not donate when his partner is) his 
partner will abandon him. 

Helping closely related organisms can appear altruistic; but this is 
also a selfish behavior. An organisms reproductive success (or 
fitness) has two components; direct fitness and indirect fitness. 
An organism's direct fitness is a measure of how many alleles it 
contributes to the subsequent generation's gene pool by 
reproducing. An organism's indirect fitness is a measure of how 
many alleles identical to its own it helps enter the gene pool. An 
organism's direct fitness plus its indirect fitness is called its 
inclusive fitness. Natural selection favors behaviors that increase 
an organism's inclusive fitness. Closely related organisms share 
many of the same alleles. For example, in  diploid species, siblings 
share at least 50% of their alleles -- the percent is higher if the 
parents are related. So, helping close relatives to reproduce gets 
an organisms own alleles better represented in the gene pool. The 
benefit of helping relatives increases dramatically in highly 
inbred species. In som  cases, organisms will completely forgo 
reproducing and only help their relatives reproduce. Ants, for 
example, have sterile castes that only serve the queen and allow 
her to reproduce. The sterile workers are reproducing by proxy. 

Keep in mind that the words "selfish" and "altruistic" have 
connotations in everyday use that biologists do not intend. 
"Selfish" simply means behaving in an attempt to maximize ones' 
own inclusive fitness; "altruistic" means behaving in an attempt to 
increase anothers fitness without regard to ones' own. This is not 
meant to imply that organisms consciously understand their 
motives. 

The opportunity for natural selection to operate does not induce 
genetic variation to appear -- selection only distinguishes 
between existing variants. Variation is not possible along every 
imaginable axis, so all possible adaptive solutions are not open to 
populations. For example, a steel shelled turtle would probably be 
an improvement. Turtles are killed quite a bit by cars these days 
because when confronted with danger, they retreat into their 
shells -- this is not a great strategy against a two ton automobile. 
However, there is no variation in metal content of shells, so it 
would not be possible to select for a steel shelled turtle.

Natural selection does not necessarily produce individually 
optimal structures or behaviors. Selection targets the organism as 
a whole, not individual traits. So, specific traits are not 
optimized, but rather combinations of traits. In addition, natural 
selection may not necessarily even select for the the most optimal 
set of traits. In any population, there would be a certain 
combination of possible alleles that would produce the most 
optimal set of traits (the global optima); but are probably several 
other sets of alleles that would yield a population almost as 
adapted (local optima). Transition from a local optima to the 
global optima may be hindered or forbidden because the population 
would have to pass through less adaptive states to make the 
transition. So, natural selection only works to bring populations to 
the nearest optimal point. 

SEXUAL SELECTION -- A SUBSET OF NATURAL SELECTION

Darwin, and others, noticed that in many species males developed 
prominent secondary sexual characteristics. A few oft cited 
examples are the peacock's tail, coloring and patterns in male 
birds in general, voice calls in frogs and flashes in fireflies. 
Many/most of these traits are a liability from the standpoint of 
survival, mainly because any ostentatious trait or noisy, 
attention-getting behavior will alert predators as well as 
potential mates. How then could natural selection favor these 
traits? 

Natural selection can be broken down into many components, of 
which survival is only one. Sexual attractiveness is a very 
important component of selection, so much so that biologists use 
the term sexual selection when they talk about this subset of 
natural selection.

Sexual selection occurs when the sexual attractiveness of a trait 
outweighs the liability incurred for survival. A male who lives a 
short time, but produces many offspring is much more successful 
than a long lived one that produces few. The former's genes will 
eventually dominate the gene pool of his species. In many species, 
especially polygynous species where only a few males monopolize 
all the females, sexual selection has caused pronounced sexual 
dimorphism. In these species males compete against other males 
for mates. The competition can be either direct (i.e. the largest 
males guarding their harems and fending off other males 
physically) or mediated by female choice.

In species where females chose, males compete by displaying 
striking phenotypic characteristics and/or performing elaborate 
courtship behaviors. The females then mate with the males that 
most interest them, usually the ones with the most outlandish 
displays. There are many competing theories as to why females are 
attracted to these displays. One model, the "good genes" model, 
states that the display indicates some component of male fitness. 
A "good genes" advocate would say that bright coloring in male 
birds indicates a lack of parasites. The females are cueing on some 
signal that is correlated with some other component of viability.

Another model, proposed by Fisher, is called the "runaway sexual 
selection" model. In his model he proposes that females may have a 
preference for some male trait (without regards to fitness) and 
then mate with these males when the trait appears. The offspring 
of these matings will therefore have the genes for both the trait 
_and_ the preference for the trait. Note, these genes would be 
expressed in the males and females respectively. As a result, the 
process snowballs out of control until natural selection brings it 
into check. Here is an example to clarify.

Suppose that, due to some quirk of brain chemistry, female birds 
of one species prefer males with longer than average tail feathers. 
Mutant males with longer than average feather will therefore 
produce more offspring than the short feathered males. In the next 
generation, the average tail feather length will increase. 

As the generations progress, feather length will increase because 
females do not prefer a specific length tail, but a longer than 
average tail. Eventually tail feather length will increase to the 
point were the liability to survival is matched by the sexual 
attractiveness of the trait and an equilibrium will be established. 
Note that in many exotic birds male plumage is often very showy 
and many species do in fact have males with greatly elongated 
feathers. In some cases these feathers are shed after the breeding 
season. 

A third model, called "the handicap hypothesis" states that males 
with the most costly displays (in terms of detriment to survival) 
are advertising the fact that, despite their "handicap", they still 
had what it took to survive. 

None of the above models are mutually exclusive. There are 
millions of sexually dimorphic species on this planet and the 
forms of sexual selection probably varies amongst them.

Natural selection is the only non-random mechanism of evolution. 
It is the only mechanism that causes adaptive evolution. The 
phrase "survival of the fittest" is often used synonymously with 
natural selection. IMHO, the phrase is both incomplete and 
misleading. For one thing, survival is only one component of 
selection -- and perhaps one of the less important ones in many 
populations. For example, in polygynous species, a number of males 
survive to reproductive age, but only a few ever mate. Males may 
differ little in their ability to survive, but greatly in their ability 
to attract mates -- the difference in reproductive success stems 
mainly from the latter consideration. Also, the word "fit" is often 
confused with physically fit. Fitness, in an evolutionary sense, is 
the average reproductive output of a class of genetic variants in a 
gene pool. Fit does not mean biggest, fastest or strongest -- 
sexiest might be closer to the truth in most animal species. 

Of all the mechanisms of evolution, natural selection has the 
potential to change gene frequencies the fastest. It usually acts to 
keep gene frequencies constant, however. This led a famous 
evolutionist, George Williams, to say "Evolution proceeds in spite 
of natural selection".

MECHANISMS OF EVOLUTION: GENETIC DRIFT

Another important mechanism of evolution is genetic drift. Drift 
is a binomial sampling error of the gene pool. What this means is, 
the alleles that form the next generation's gene pool are a sample 
of the alleles from the current generation.

Drift is a rather abstract concept to some; I will try to explain it 
via an analogy. Imagine you had a swimming pool full of one 
million marbles (this will represent the parental gene pool), half 
are red and half are blue. If you repeatedly picked ten marbles out, 
do you think you would get five red and five blue every time 
(assume you replaced your sample to the pool each time)? If you 
picked one hundred marbles out, do you think you would get fifty 
red and fifty blue out every time? In both cases the answer is no, 
some times the frequency of red marbles in the sample would 
deviate from 0.50. In the case of the 100 marble sample, the 
frequency of red marbles would deviate much less, however.

If, after picking out ten or one hundred marbles, you refilled the 
pool with marbles at the frequency of that sample and repeated 
the process over and over; what do you think would happen? What 
would happen is that the frequency of red to blue would fluctuate 
over time. Eventually, there would be only one color marble left in 
the pool. This is roughly analogous to how genetic drift works.

In small populations, the rate of change in the frequency of alleles 
is greater than in large populations. However, the overall rate of 
genetic drift is independent of population size. If the mutation 
rate is constant, large and small populations lose alleles to drift 
at the same rate. This is because large populations will have more 
alleles in the gene pool, but they will lose them more slowly. 
Smaller populations will have fewer alleles, but these will quickly 
cycle through. This assumes that selection is not operating on any 
of these alleles.

Sharp drops in population size can greatly affect the gene pool. 
When a population crashes, the alleles in the surviving sample may 
not be representative of the pre-crash gene pool. This change in 
the gene pool is called the founder effect, because small 
populations of organisms that invade a new territory (founders) 
are subject to this. Many biologist feel the genetic changes 
brought about by founder effects may contribute to isolated 
populations developing reproductive isolation from their parent 
populations. 

Both natural selection and genetic drift decrease genetic 
variation. If they were the only mechanisms of evolution, 
populations would eventually become homogeneous and further 
evolution would be impossible. There are, however, mechanisms 
that replace variation depleted by selection and drift. These are 
discussed below.

MECHANISMS THAT INCREASE GENETIC VARIATION
------------------------------------------
MECHANISMS OF EVOLUTION: MUTATION

A mutation is a change in a gene. There are many kinds of 
mutations. A point mutation is a mutation in which one "letter" of 
the genetic code is changed to another. Lengths of DNA can also be 
deleted or inserted in a gene; these are also mutations. Finally, 
genes or parts of genes can become inverted or duplicated. 

Mutation is a mechanism of evolution because it changes allele 
frequencies very slightly. If an allele "A" mutates to another allele 
"a", the frequency of "a" has increased from zero to some small 
number (1/2N in a diploid population where N is the effective 
population size). The allele "A" will also decrease slightly in 
frequency. Evolution via mutation alone is very slow; for the most 
part, mutation just supplies the raw material for evolution -- 
genetic variation. 

Most mutations are slightly deleterious or neutral. The genome of 
most organisms (certainly all eukaryotes) contains enormous 
amounts of junk sequences. In addition, even in coding regions, 
many sites can undergo mutation and still maintain the original 
meaning. In other words, the genetic code is redundant. So, most 
mutations are neutral or nearly so; but, the overwhelming majority 
of mutations that produce any detectable phenotypic effect are 
deleterious. "Good" mutations, however, do occur.

One example of a beneficial mutation comes from the mosquito 
_Culex_ _pipiens_. In this organism, a gene that was involved with 
breaking down organophosphates - common insecticide ingredients 
- became duplicated. Progeny of the organism with this mutation 
quickly swept across the worldwide mosquito population. There 
are numerous examples of insects developing resistance to 
chemicals, especially DDT - which was once heavily used in this 
country. And, most importantly, even though "good" mutations 
happen much less frequently than "bad" ones, organisms with 
"good" mutations thrive while organisms with "bad" ones die out. 

Mutations occur at random with respect to their adaptive 
significance. Organisms cannot "decide" that they need a mutation 
and have it occur. The frequency of a mutation occurring is 
independent of the potential effect it would have, with one 
exception. 

A new class of mutation has recently been documented in bacteria
and yeast. It appears that unicellular organisms can undergo 
directed mutagenesis to repair "broken genes". The reversion 
mutation that restores a gene to normal functioning occurs several 
orders of magnitude more frequently when the gene is needed than 
when it isn't. The mechanism of directed mutagenesis is unknown 
at this time, but it has been shown to be under genetic control - - 
i.e. directed mutations are not errors like normal mutations are; 
they are actively created (or selectively retained) by the organism 
in response to the environment. 

The importance of directed mutagenesis is not yet known. 
Biologists have not yet studied if directed mutations can produce 
novel solutions to environmental challenges. It is also unknown if 
it can occur in multi-cellular organisms with separate germ and 
somatic cell lines. In any case it appears that in at least a few 
instances, the potential for selection to operate induces adaptive 
genetic variation to appear. 

MECHANISMS OF EVOLUTION: RECOMBINATION 

Recombination can be thought of as gene shuffling. Most organisms 
have linear chromosomes and their genes lie at specific location 
(loci) along them (bacteria have circular chromosomes). In most 
sexually reproducing organisms, there are two of each chromosome 
type in every cell. For instance in humans, there are two 
chromosomes number one (through 22 and two sex chromosomes), 
one inherited from the mother, the other inherited from the father. 
When an organism produces gametes, the gametes end up with only 
one of each chromosome per cell. Haploid gametes are produced 
from diploid cells by a process called meiosis. 

In meiosis, homologous chromosomes line up. The DNA of the 
chromosome is broken on both chromosomes in several places and 
rejoined with the other strand. Later in meiosis, the two 
homologous chromosomes are split into two separate cells that 
divide and become gametes. But, because of recombination, both of 
the chromosomes are a mix of alleles from the mother and father. 
For example, let's say an organism has a chromosome with three 
genes, (A,B and C -- in that order). Assume that at each of these 
three loci there are at least two alleles. From the father, the 
organism inherited a chromosome with the alleles A1, B1 and C1. 
From the mother the organism inherited A2,B2 and C2 alleles. In 
meiosis the two chromosomes would line up and the two A alleles 
would line up, as would the B and C alleles. If recombination 
occurred between locus A and locus B, the resulting chromosomes 
in the two gametes would be; one chromosome carrying A1, B2 and 
C2 alleles and one chromosome carrying A2, B1 and C1 alleles.

Real chromosomes carry many more than three genes and 
recombination occurs at many locations along the chromosome. The 
end result is that the two homologous chromosomes have 
"shuffled" alleles. 

Recombination can occur not only between genes, but within genes 
as well. Recombination within a gene can form a new allele. 
Recombination is a mechanism of evolution because it adds new 
alleles and combinations of alleles to the gene pool. 

A beneficial aspect of recombination is that beneficial mutants 
can be brought together onto the same chromosome, even if they 
arose in separate organisms. 

MECHANISMS OF EVOLUTION: GENE FLOW 

Gene flow simply means new genes added to a population by 
migration from another population. In some closely related 
species, fertile hybrids can result from interspecific matings. 
These hybrids can vector genes from species to species. 
Gene flow between more distantly related species occurs 
infrequently. One interesting case of this involves genetic 
elements called P elements. In the genus _Drosophila_, P elements 
were transfered from some species in the _willistoni_ group, to 
_D. melanogaster_. These two species of fruit flies are distantly 
related and hybrids do not form. Their ranges do, however, overlap. 
The P elements were vectored into _D. melanogaster_ via a 
parasitic mite that targets both these species. This mite 
punctures the exoskeleton of the flies and feeds on the "juices". 
Material, including DNA, from one fly can be transfered to another 
when the mite feeds. Since P elements actively move in the 
genome (they are themselves parasites of DNA), one incorporated 
itself into the genome of a _melanogaster_ fly and subsequently 
spread through the species. Laboratory stocks of _melanogaster_ 
caught prior to the 1940's are devoid of P elements. All natural 
populations today harbor them.

OVERVIEW OF EVOLUTION WITHIN A LINEAGE (ANAGENESIS)

--------------------------------------------------- 

Evolution is a change in the gene pool of a population over time; it 
can occur due to several factors. Three mechanisms add new 
alleles to the gene pool: mutation, recombination and gene flow. 
Two mechanisms remove alleles, genetic drift and natural 
selection. Drift removes alleles randomly from the gene pool. 
Selection removes deleterious alleles from the gene pool. Natural 
selection can also increase the frequency of an allele (or 
combination of alleles) in the gene pool. Selection that weeds out 
harmful alleles is called negative selection. Selection that 
increases the frequency of helpful alleles is called positive, or 
sometimes positive Darwinian, selection. 

A new allele can also drift to high frequency. But, since the change 
in frequency of an allele each generation is random, nobody speaks 
of positive or negative drift. 

Except in rare cases of high gene flow, all new alleles enter the 
gene pool as a single copy. Most new alleles added to the gene pool 
are lost almost immediately due to drift or selection; only a small 
percent ever reach a high frequency in the population. Even most 
moderately beneficial alleles are lost due to drift when they 
appear. 

The fate of any new allele depends a great deal on the organism it 
appears in. This allele will be linked to the other alleles near it 
for many generations. A mutant allele can increase in frequency 
simply because it is linked to a beneficial allele at a nearby locus. 
This can occur even if the mutant allele is deleterious, although it 
must not be so deleterious as to offset the benefit of the other 
allele. Likewise a potentially beneficial new allele can be 
eliminated from the gene pool because it was linked to deleterious 
alleles when it first arose.


An allele "riding on the coat tails" of a beneficial allele is called a 
hitchhiker. Eventually, recombination will bring the two loci to 
linkage equilibrium. But, the more closely linked two alleles are, 
the longer the hitchhiking will last. 

The effects of selection and drift are coupled. Drift is intensified 
as selection pressures increase. This is because increased 
selection (i.e. a greater difference in reproductive success among 
organisms in a population) reduces the effective population size, 
the number of individuals contributing alleles to the next 
generation. 

Adaptation is brought about by cumulative natural selection, the 
repeated "sifting" of mutations by natural selection. Small 
changes, favored by selection, can be the stepping-stone to further 
changes. The summation of large numbers of these changes is 
macroevolution. This is discussed below.

EVOLUTION AMONG LINEAGES (CLADOGENESIS) 

The following sections deal with how single populations ramify to 
become multiple populations and eventually separate species - 
this is called cladogenesis. In edition, the overall pattern of 
macroevolution and evidence for common descent of all living 
species is presented.

THE PATTERN OF MACROEVOLUTION 

Evolution is not progress. The popular notion that evolution can be 
represented as a series of improvements from simple cells, 
through more complex life forms, to humans (the pinnacle of 
evolution), can be traced to the concept of the scale of nature. This 
view is incorrect.
Modern biologists hold that all species have descended from a 
common ancestor. As time went on, different lineages of 
organisms were modified with descent to adapt to their 
environments. Thus, evolution is best viewed as a branching tree 
or bush, with the tips of each branch representing currently living 
species. No living organisms today are our ancestors. Every living 
species is as fully modern as we are with its own unique 
evolutionary history. No extant species are "lower life forms", 
atavistic stepping stones paving the road to humanity. 

A related, and common, fallacy about evolution is that humans 
evolved from living species of apes. This is not the case -- humans 
and apes share a common ancestor. Both humans and living apes are 
fully modern species; the ancestor we evolved from is now extinct 
and was not the same as present day apes (or humans for that 
matter). Our closest relatives are the chimpanzee and the pygmy 
chimp.        

EVIDENCE FOR COMMON DESCENT AND MACROEVOLUTION

---------------------------------------------

Whereas microevolution can be studied directly, macroevolution is 
studied by examining patterns in biological populations and clades 
(groups of organisms) and inferring process from pattern. Given 
the observation of microevolution and the knowledge that the 
earth is billions of years old -- macroevolution could be 
postulated. But this extrapolation, in and of itself, does not really 
provide a compelling explanation of the patterns of biological 
diversity we see today. Evidence for macroevolution, or common 
ancestry and modification with descent, comes from several other 
fields of study. These include: comparative biochemical and 
genetic studies, comparative developmental biology, patterns of 
biogeography, comparative morphology and anatomy and the fossil 
record. 
Comparative genetic and biochemical data provide data supporting 
the inference of common descent. DNA sequence comparisons of 
closely related species (as determined by morphologists) yeild 
similar sequences. Overall sequence similarity is not the whole 
story, however. The pattern of differences we see in closely 
related genomes is worth examining.

Genes are sequences of nucleotides that code for proteins. There 
are four different kinds of nucleotides commonly incorporated into 
DNA: adenine (A), guanine (G), cytosine (C) and thymine (T) -- each 
block of three is called a codon. Each codon designates an amino 
acid (the subunits of proteins). The gene, or sequence of codons, is 
transcribed into RNA -- a nucleic acid similar to DNA. (RNA, like 
DNA, is made up of nucleotides although the nucleotide uracil (U) 
is used in place of thymine (T).) The RNA is then translated via 
cellular machinery into a string of amino acids -- a protein. 

All living organisms use DNA as their genetic material, although 
some viruses use RNA. The three letter code is the same for all 
organisms. The universal genetic code is redundant. There are 64 
codons, but only 20 amino acids to code for; so, most amino acids 
are coded for by several codons. In many cases the first two 
nucleotides in the codon designate the amino acid. The third 
position can have any of the four nucleotides and not effect how 
the code is translated.

In addition to showing overall similarity, gene sequences from 
closely related species show the same codon is often used for 
amino acids. In cases where there are differences, however, they 
are usually in these "silent" sites. In addition, the genome is 
loaded with 'dead genes' called pseudo-genes. Pseudogenes occupy 
the same location in the genome in closely related species. The 
same can be said for introns, sequences of DNA that interrupt a 
gene, but do not code for anything. Introns are spliced out of the 
RNA prior to translation, so they do not contribute information 
needed to make the protein. They are sometimes, however, involved 
in regulation of the gene.

Third codon positions (silent sites), pseudo-genes and introns 
show more sequence differences between species than coding 
sections of a gene. This is because mutations that change the code 
of a gene, and hence the protein made, usually affect the organism 
adversely and are selected against. Mutations in non-coding 
regions do not affect the phenotype of the organism and get passed 
on.

If two species shared a recent common ancestor one would expect 
genetic information, even information such as redundant 
nucleotides and the position of introns or pseudogenes, to be 
similar. Both species would have inherited this information from 
their common ancestor. The degree of similarity would be a 
function of divergence time.

Studies in comparative anatomy also provide support for common 
descent. Groups of related organisms are 'variations on a theme' -- 
the same set of bones are used to construct all mammals. The 
bones of the human hand grow out of the same tissue the bones of 
a bat's wing or a whale's flipper does and they share many 
identifying features (muscle insertion points, ridges).  The only 
difference is that they are scaled differently. Evolutionary 
biologists say this indicates that all mammals are modified 
descendents of a common ancestor which had the same set of 
bones.

Evidence for common descent also comes from studying 
comparative developmental biology-- Closely related organisms 
share similar developmental pathways, the differences in 
development are most evident at the end. This is, again, usually 
illustrated using mammalian (or sometimes vertebrate) examples. 
As organisms evolve, their developmental pathway gets modified. 
It is easier to modify the end of a developmental pathway than the 
beginning since changes early on have a cascading effect. 
Therefore, organisms pass through stages of early development 
that their ancestors passed through. These stages, however, are 
modified because selection "sees" all phases of an organism's life 
cycle. So, an organism's development mimics its ancestors 
although it doesn't recreate it exactly.

Traces of an organism's ancestry sometimes remain even when an 
organisms ontogeny (development) is complete. These are called 
vestigal structures. Many snakes have rudimentary pelvic bones 
retained from their walking ancestors. This is an example of a 
vestigal structure.

Biogeography also supports the inference of common descent. 
Organisms clustered spatially are frequently also clustered 
phylogenetically; this is especially true of organisms with limited 
dispersal opportunities. The mammalian fauna of Australia is 
often cited as an example of this; marsupial mammals fill most of 
the equivalent niches that placentals fill in other ecosystems. If 
all organisms descended from a common ancestor, species 
distribution across the planet would be a function of site of 
origination, potential for dispersal and time since origination. In 
the case of Australian mammals, their physical separation from 
sources of placentals means potential niches were filled by a 
marsupial radiation rather than a placental radiation or invasion.

Natural selection can only mold available genetically based 
variation. In addition, natural selection provides no mechanism for 
advance planning. If selection can only tinker with what it has to 
work with and, if all organisms share a common ancestor, we 
should expect to see examples of suboptimal design in living 
species. This is indeed the case.

In African locusts, the nerve cells that connect to the wings 
originate in the abdomen, even though the wings are in the thorox. 
When the insect send the message to fly from its brain to its 
wings, the nerve impulse travels down the ventral nerve cord past 
its target then backtracks to the wing.

In _Cnenidophoran_ lizards, females reproduce 
parthenogenetically. Fertility in these lizards is increased when a 
female mounts another female and simulates copulatory behavior. 
This is because these lizards evolved from sexual lizards whose 
hormones were aroused by sexual behavior. Now, although the 
sexual mode of reproduction has been lost, the means of getting 
aroused (and hence fertile) has been retained. 

Fossils show hard structures of organisms less and less similar to 
modern organisms as you go down the strata (layers of rocks). In 
addition, patterns of biogeography apply to fossils as well as 
extant organisms. When combined with plate tectonics, fossils 
provide evidence of distributions and dispersals of ancient 
species. For example, South America had a very distinct marsupial 
mammalian fauna until the land bridge formed between North and 
South America. After that marsupials started disappearing and 
placentals took their place. This is commonly interpreted as the 
placentals wiping out the marsupials (but this may be an over 
simplification).

Further strong evidence for macroevolution comes from the fact 
that suites of traits in biological entities fall into a nested 
pattern. For example, plants can be divided into two broad 
categories, non-vascular (mosses) and vascular. Vascular plants 
can be divided into seedless (ferns) and seeded. Vascular seeded 
plants can be divided into gymnosperms (pines) and flowering 
plants or angiosperms. And angiosperms can be divided into 
monocots and dicots. Each of these types of plants have several 
characters that distinguish them from other plants -- traits are 
not "mixed and matched" in groups of organisms. For example, 
flowers are only seen in plants that carry several other characters 
that distinguish them as angiosperms. This pattern arises due to 
lineages splitting (speciation), retaining ancestral traits and 
deriving new traits. Derived traits only appear in lineages 
descended from the population that first displayed the trait. This 
hierarchical pattern of diversity is what one expects to see if 
species branch into new species and are modified with descent. 

Thus, it is not just that similar species share similar traits 
(although that is evidence in and of itself); when you look at large 
groups of organisms, a pattern on a larger scale is seen. This 
hierarchical pattern can be produced even if the process 
responsible is not hierarchical. For example, microevolution leads 
to hierarchical patterns of genetic diversity even though it works 
at a single level. The question of hierarchical processes in 
evolution is still being debated. 

The real test of any scientific theory, is its ability to generate 
testable predictions and, of course, have the predictions borne out. 
Evolution easily meets this criteria. In several of the above 
examples I stated, closely related organisms share X. If I define 
closely related as sharing X, this is a contentless statement. It 
does however, provide a prediction. If two organisms share (oh 
lets say) a similar anatomy (two birds, for ex.), I would then 
predict that their gene sequences would be more similar than a 
morphologically distinct organism (like a plant, for ex.). This has 
been spectacularly borne out by the recent flood of gene sequences 
-- the correspondence to trees drawn by morphological data is 
very high. The discrepancies are never too great and usually 
confined to cases where the pattern of relationship was hotly 
debated. 

SCIENTIFIC STANDING OF EVOLUTION AND IT'S CRITICS

The topics of evolution and common descent were once highly 
controversial in scientific circles; this is no longer the case. 
Although debates rage about how various aspects of evolution 
work and details of patterns of relationships are not fully worked 
out, evolution and common descent are considered fact by the 
scientific community. 

So-called "scientific" creationists do not base their objections on 
scientific reasoning or data. Nor do they have a testable, scientific 
theory to replace evolution with. "Scientific creationism" is a 
poorly disguised attempt to attack evolution because it 
contradicts the religious beliefs of some fundamentalists. 

SPECIATION -- INCREASING BIOLOGICAL DIVERSITY
--------------------------------------------- 

Speciation is the process of a single species becoming two or 
more species. Many biologists feel speciation is key to 
understanding evolution and that certain evolutionary phenomena 
apply only at speciation and macroevolutionary change cannot 
occur without speciation. Other biologists think major 
evolutionary change can occur without speciation. Changes 
between lineages are only an extension of the changes within each 
lineage. In general, paleontologists fall into the former category 
and geneticists in the latter. 

MODES OF SPECIATION 
Biologists recognize two types of speciation: allopatric and 
sympatric speciation. The two differ in geographical distribution 
of the populations in question. 

Allopatric speciation is thought to be the most common form of 
speciation. It occurs when a population is split into two (or more) 
geographically isolated subdivisions that organisms cannot bridge. 
Eventually, the two populations' gene pools change independently 
until they could not interbreed even if they were brought back 
together. In other words, they have speciated. 

Sympatric speciation occurs when two subpopulations become 
reproductively isolated without first becoming geographically 
isolated. Monophytophagous insects (insects that live on a single 
host plant) provide a model for sympatric speciation. If a group of 
insects switched host plants they would not breed with other 
members of their species still living on their former host plant. 
The two subpopulations could diverge and speciate. Some 
biologists call sympatric speciation microallopatric speciation to 
emphasize that the subpopulations are still physically separate at 
an ecological level.

Biologists know little about the genetic mechanisms of speciation. 
Some think series of small changes in each subdivision gradually 
lead to speciation; others think there may be a few key genes that 
could change and confer reproductive isolation. One famous 
biologist thinks most speciation events are caused by changes in 
internal symbionts. Most doubt this, however. Populations of 
organisms are very complicated. It is likely that there are many 
ways speciation can occur. Thus, all of the above ideas may be 
correct, each in different circumstances. 

OBSERVED SPECIATIONS 

It comes as a surprise to some to hear that speciation has been 
observed. In the genus _Tragopogon_ (a plant genus consisting 
mostly of diploids), two new species (_T._ _mirus_ and _T._ 
_miscellus_) have evolved within the past 50-60 years. The new 
species are allopolyploid descendants of two separate diploid 
parent species. 

Here is how this speciation occured. The new species were formed 
when one diploid species fertilized a different diploid species and 
produced a tetraploid offspring. This tetraploid offspring could not 
fertilize or be fertilized by either of its two parent species types. 
It is reproductively isolated, the definition of a species. 

Two other plant species have also arisen within the past 110 
years in this manner, _Senecio_ _cambrensis_ and _Spartina_ 
_townsendii_.

EXTINCTION -- DECREASING BIOLOGICAL DIVERSITY

--------------------------------------------- 

"ORDINARY" EXTINCTION 

Extinction is the ultimate fate of all species. The reasons for 
extinctions are numerous. A species can be outcompeted by a 
closely related species, the habitat a species lives in can 
disappear and/or the organisms that the species exploits could 
come up with an unbeatable defense. 

Some species enjoy a long tenure on the planet while others are 
short-lived. Some biologists believe species are "programmed" to 
go extinct in a manner analogous to organisms being destined to 
die. The majority, however, believe that if the environment stays 
fairly constant, a well adapted species could continue to survive 
indefinitely.

MASS EXTINCTION

Mass extinctions shape the overall pattern of macroevolution. If 
you view evolution as a branching tree, it's best to picture it as 
one that has been severely pruned a few times in its life. The 
history of life on this earth includes many episodes of mass 
extinction in which many taxa (groups of organisms) were wiped 
off the face of the planet. Mass extinctions are followed by 
periods of radiation where new species evolve to fill the empty 
niches left behind. It is probable that surviving a mass extinction 
is largely a function of luck. Thus contingency plays a large role in 
patterns of macroevolution. 

The most famous extinction occurred at the boundary between the 
Cretaceous and Tertiary Periods (the K/T Boundary- 65MYA). This 
extinction eradicated the dinosaurs. Some hypothesize that the 
K/T event was caused by environmental disruption brought on by a 
large impact on earth. Several lines of evidence point to a large 
collision at the time of the extinction, but attempts to link the 
two have not been convincing to all biologists. Following this 
extinction the mammalian radiation occurred. Mammals coexisted 
for a long time with the dinosaurs but were confined mostly to 
nocturnal insectivore niches. With the eradication of the 
dinosaurs, mammals radiated to fill the vacant niches.

The largest mass extinction came at the end of the Permian 
(250MYA); it is estimated that 96 percent of all species died out 
at this time. The sea animals that make up the so-called Paleozoic 
Fauna (among them crinoids, cephalopods, brachiopods and corals), 
suffered the worst. This assemblage did not reradiate after the 
event and remains at the level of diversity it sunk to after the 
extinction. In contrast, the sea animals that make up the Modern 
Fauna (gastropods, bivalves, crabs, echinoids and bony fishes) 
were barely affected and continued to increase in diversity after 
the event.

The Permian extinction coincides with the formation of Pangea II, 
when all the world's continents were brought together by plate 
tectonics. A worldwide drop in sea level also occurred at this 
time. Currently, human alteration of the ecosphere is causing a 
global mass extinction. 

PUNCTUATED EQUILIBRIA 

---------------------
Some paleontologists believe evolution is a hierarchical process. 
The theory of punctuated equilibria attempts to infer the process 
of macroevolution from the pattern of species documented in the 
fossil record. In the fossil record, transition from one species to 
another is usually abrupt in most geographic locales -- no 
transitional forms are found. In short, it appears that species 
remain unchanged for long stretches of time and then are quickly 
replaced by new species. However, if wide ranges are searched, 
transitional forms that bridge the gap between the two species 
are sometime found in small, localized areas.

For example, in Jurassic brachiopods of the genus _Kutchithyris_, 
_K. acutiplicata_ appears below another species, _K. euryptycha_. 
Both species were common and covered a wide geographical area. 
They differ enough that some have argued they should be in a 
different genera. In just one small locality an approximately 
1.25m sedimentary layer with these fossils is found. In the narrow 
(10 cm) layer that separates the two species, both species are 
found along with transitional forms. In other localities there is a 
sharp transition. 

Gould and Eldredge, the authors of punctuated equilibria, interpret 
this in light of theories of allopatric speciation. They concluded 
that isolated populations of organisms will often speciate and 
then invade the range of their ancestral species. Thus at most 
locations that fossils are found, transition from one species to 
another will be abrupt. This abrupt change will reflect 
replacement by migration however, not evolution. In order to find 
the transitional fossils, the area of speciation must be found. 

They also argue that evolution can proceed quickly in small 
populations so that the tempo of evolution is not continuous. This 
has lead to some confusion about the theory. Some popular 
accounts give the impression that abrupt changes in the fossil 
record are due to blindingly fast evolution; this is not what the 
theory of punctuated equilibria says. 

Some PE proponents envision the theory as a hierarchical theory of 
evolution because they see speciation as analogous to mutation 
and the replacement of one species by another (which they call 
species selection) as analogous to natural selection. Speciation 
adds new species to the species pool just as mutation adds new 
alleles to the gene pool and species selection favors one species 
over another just as natural selection can favor one allele over 
another. This is the most controversial part of the theory. Most 
biologists agree with the pattern of macroevolution these 
paleontologists posit, but many disagree with the mechanism -- 
species selection. Critics would argue that species selection is 
not analogous to natural selection and therefore evolution is not 
hierarchical.

The theory of punctuated equilibrium was designed to replace the 
theory of phyletic gradualism. Phyletic gradualists held that a 
species would slowly transform into another species over its 
entire range. Phyletic gradualism is often associated with the 
assumption of a uniform rate of evolution, but this need not be the 
case. 

CONCLUSION 

----------

ARE WE STILL EVOLVING?

Yes, evolution is still occurring; all organisms continue to adapt to 
their surroundings and "invent" new ways of better competing with 
members of their own species. In addition, allele frequencies are 
being changed by drift, mutation and gene flow constantly. 
Studying the process of evolution as it continues to occur is a 
major field of biology today. Although evolution has been observed 
and all the mechanisms have been shown to work, there is still no 
consensus on the relative contribution of each of the mechanisms 
to the overall pattern of evolution within a lineage. Likewise, 
although new species have been seen to arise; biologists have 
many questions about what influences the pattern of 
macroevolution. Are some groups "good" at speciating? Who 
survives mass extinctions and why? 

Evolution is the unifying theory of biology. The functions of 
biological entities at all levels (populations, organisms, genes) 
are the product of a non-random factor (e.g. natural selection) 
operating in conjunction with random factors (such as mutation 
and mass extinction) within a framework of historical constraint. 
For centuries humans have asked, "Why are we here?". A question 
such as that probably lies outside the realm of science. However, 
biologists can provide an elegant answer to the question, "How did 
we get here?" 

--------------------------------------------------------------------

SOME GOOD EVOLUTION TEXTS (IMHO) 

A good introductory text in evolutionary biology is: 
Evolutionary Biology, by Douglas Futuyma, 1986, Sinauer, Sunderland, Mass
 The text assumes some previous knowledge of biology, but reviews most 
critical background material. It contains numerous references to the 
primary 
literature. Most of the information in this file can be found (along with the 
references to the primary literature) in this text. 

A good introductory text into population genetics, the field that 
mathematically describes changes in the gene pool is:
 Principles of Population Genetics, by Hartl and Clark , 1989, Sinauer, 
Sunderland, Mass
None of the math is very daunting (it's just an intro text after all)
but it's really critical (IMHO) to understanding what evolution is all about. 
And again, lots of refs. 

A text that deals with the interface of molecular biology and evolution is: 
Fundamentals of Molecular Evolution, by Li and Graur, 1991, Sinauer, 
Sunderland, Mass 
A very concise introduction to this field. 

A text that deals with theories of macroevolution is: 
 Macroevolutionary Dynamics, by Niles Eldredge, 1989, McGraw-Hill, New 
York

 A text that documents the history of life on earth is: 
History of Life, by Richard Cowen, 1990, Blackwell Scientific, Boston 
A readable introduction to the history of our planet and especially the 
changes that have occurred in the biota. 

A popular introduction to the field that also debunks the most common 
creationist arguments is:
 The Blind Watchmaker, by Richard Dawkins, 1987, Norton, New York 
Dawkins is (IMHO) a very engaging writer. 

A close look at the creation/evolution debate can be found in: 
Abusing Science, by Philip Kitcher, 1982, MIT, Cambridge, Mass 
A meticulous critique of creationism. 

======================================================================

Author: Chris Colby (colby@bu-bio.bu.edu)
 Title: Evidence for Evolution FAQ

======================================================================

    This is a compilation of my "evidence for evolution"
posts to talk.origins. It is not in any particular order
because each post can stand on it's own. The intro and
data section for #2 are, however, split up.

Chris Colby
email: colby@bu-bio.bu.edu

************************************************************************


Subject: evidence for evolution (1)
Summary: a look at cichlid fish in Lake Victoria

        This is the first in what I hope to be a series of postings. In
the series I hope to accomplish two things, establish that evolution
is an active branch of mainstream science and that there is indeed
an overwhelming amount of evidence in favor of the idea of evolution.
Note that no single post is meant to be a proof, just another piece
of evidence that supports the theory of evolution.

        In the October 11th (1990) issue of Nature, Meyer et.al. present
of paper aimed at establishing if the cichlid fish species of Lake
Victoria (Africa) are monophyletic or polyphyletic. (If they all
share a recent common ancestor in that lake or came from separate
lineages that invaded the lake). In their paper they sequenced a
363 bp part of the cytochrome b gene and a 440 bp segment of
mitochondrial DNA from what is called the control region. They
sequenced these genes from several species of fish in the lake
and a few species from relatively nearby lakes.

        What they found was the sequences in the Lake Victoria
species of fish were all very similar, but they were different from
the sequences of fish in nearby lakes. All the sequences are listed
in the paper.

        They came to the conclusion that this indicated the cichlid
species of Lake Victoria all derive from a recent common ancestor
in the lake. They estimate the time of divergence at about 200,000
years ago based on a model that assumes mutations are relatively
constant over time. (The lake, incidentally, had been independently
dated to be 250,000 - 275,000 years old)

        The News and Views section of that issue has an overview
of the paper written by John Avise. Also, the cover photo of this
issue consists of a picture of several of these fish.

REFERENCE:

Meyer, et. al., 1990, Monophyletic origin of Lake Victoria cichlid
fishes suggested by mitochondrial DNA sequences, Nature 347: 550-553

************************************************************************

Subject: evidence for evolution (6-intro)
Summary: sexual selection

Keywords: good genes, runaway sexual selection

    colby@bu-bio.bu.edu 

    In this post I present two models of sexual selection and a
paper that tests one of the predictions of both models. The first
article in the post will be an exposition of the theory and the
second article will be a discussion of the paper.

    Darwin, and others, noticed that in many species males devel-
oped prominent secondary sexual charactoristics. A few oft cited ex-
amples are the peacocks tail, coloring and patterns in male birds in
general, voice calls in frogs and flashes in fireflies. Many/most of
these traits are a liability from the standpoint of survival, mainly
because an ostentatious display to attract females is also going
to catch to the eyes/ears/nose/whatever of predators. How then could
natural selection favor these traits? Well, as I pointed out in a pre-
vious post, the sexual attractiveness of these traits outweighs the
liability incurred for survival. A male who lives a short time, but
produces many offspring is much more successful than a long lived one
that produces few. His genes will eventually dominate the gene pool of
his species.

    There are two competing theories as to why females are attract-
ed to male displays. One model, the "good genes" model, states that the
display indicates some component of male fitness. A "good genes" advo-
cate would say that bright coloring in male birds indicates a lack of
parasites. The females are cueing on some signal, in this example color,
that is correlated with some other important trait (ex. parasite load).

    The second model, proposed by Fisher, is called the "runaway
sexual selection" model. In his model he proposes that females develop
a preference for some male trait (without regards to fitness) and then
mate with these males. The offspring of these matings will therefore
have the genes for both the trait _and_ the preference for the trait.
Note, these genes would be expressed in the males and females respect-
ively. As a result the process snowballs out of control until natural
selection brings it into check. An example to clarify.

     Suppose, due to some quirk of brain chemistry, female birds
of one species prefer males with longer than average tail feathers.
Males in the population with longer than average feather will there-
fore produce more offspring than the short feathered males. So in
the next generation, the average tail feather length will increase.
As the generations progress, tail feather length will increase becuase
females prefer not a specific length tail, but tails a little longer
than average. Eventually tail feather length will increase to the
point were the liability to survival is matched by the sexaul attract-
iveness of the trait and an equilibrium will be established. Note
that in many exotic birds male plumage is often very showy and many
species do in fact have males with greatly elongated feathers. In
some cases these feathers are shed after the breeding season.

    In both of these models, which are not mutually exclusive, it
is predicted that female mating preference will be correlated with
the male trait. In the first case because the trait is a signal for
some other, underlying benificial trait. In the second case because
the the genes for the trait and preference for the trait are, or
become linked.

    In the paper I will present, the authors test this prediction.
Their paper is not an attempt to discriminate between these two models.
If the common prediction of both of these models turned out to be
false, then both the models would have to be given the boot. That is
the justification for the study.

Subject: evidence for evolution (6-data)
Summary: trait correlates with preference
Keywords: male trait, female preference

    In the paper I discuss here, the authors (Houde and Endler,1990)
conduct experiments on the guppy _Poecilia_ _reticulata_. They collected
these fish from 7 different streams that harbor these species. Each
stream differed in the color pattern of male fish residing there. Male
guppies had orange coloring covering from between 5% to 17% of their body,
depending on which stream they came from.

    They experimented by placing 6 males and 6 females in a tank
and measuring the sexual attractiveness of the males. This was calc-
ulated as percentage of male displays that elicited a response from
the female. In each separate experiment all the males were from one
locale and all the females were from the same or another locale. They
tested most, but not all, of the possible combinations of male/females.

    They found that, female guppies from streams where males
had large amounts of orange coloring strongly prefered male
guppies with large amounts of orange to males with less orange. In
populations where males had low amounts of orange coloring the
females had no real preference with respect to coloring. The
preference exhibited by females in the first sentence was, of
course, statistically significant.

    They interpreted this as, in the populations where coloring
is prominant, evolution of female preference is correlated with the
evolution of the male trait. In the populations where coloring is
less prominant, there is no association between the male trait and
the female preference.

    The authors also mention a few factors that may confuse the
issue. It had previously been shown that females in lightly predated
waters favored brightly colored males more than females in heavily
predated water.

    In addition, a similar experiment by Kodrick and Brown had
shown that females _always_ prefered prominantly colored males. They
point out however, that these fish were from highly inbred lab stocks
whereas Houde and Endler used fish recently sampled from nature 
(all the fish were less than three generations removed from the wild).

    To conclude, the authors reach the conclusion that female
preference and male trait are correlated in populations where the
male triat is prominent. This was a prediction of both the "good
genes" and the "runaway sexual selection" model.

REFERENCE:

Houde and Endler, 1990, Correlated Evolution of Female Mating
Preferences and Male Color Pattern in the Guppy _Poecilia_ _reticulata_,
Science 248: 1405 - 1408

Subject: evidence for evolution (7)
Summary: sperm competition in 13 lined ground squirrels
Keywords: sperm competition

    Here's number seven in my series. It's about sperm compe-
tition and male mate choice in 13 lined ground squirrels. As I
have said before, each post is just the summary of some current
paper published in a mainstream peer reviewed journal. This shows
that evolutionary biology is a valid. productive branch of science
and is recognized as such by the scientific community as a whole.
No article is meant as a capsule proof of evolution.

    In most species, females choose the males they wish to mate
with. This is not the case in the thirteen lined ground squirrel,
_Spermophilus_ _tridecemlineatus_. In this system, oestrous females
mate with any male that approaches them. On average a female will
have two matings. The first male to mate will sire more of the
offspring than the second (this is due to sperm competition). The
ratio of first male offspring to second male offspring is modulated
by two factors: delay between matings and duration of second mating.
The longer the delay between the first and second mating, the less
offspring the second male will sire. He can increase this number,
however, by increasing copulatory time.

    So, when a male arrives at a female who is already being 
courted he has two choices. (note, the first male on the scene is
always the first to mate) He can wait until the first male leaves,
or attempt to find a new female (hopefully an unmated one). As it
turns out, females are scarce enough that it usually pays for the
second male to wait. Siring fewer offspring is preferable to not
finding a mate and siring none. However, males had been observed
in the field rejecting certain females (ones who had mated awhile
earlier) and searching for a new mate rather than going for the
sure copulation.

    The authors worked out a mathematical model (a fairly
simple one) that showed, after a long enough time has passed 
since the first mating, the second male is going to sire a negligible
amount of the female litter (due to sperm competition, remember the first
male sires more and the proportion gets larger as time goes on). In this
case the probability (although low) of producing offspring from an
unmated female that he still has to go locate is greater than the
probability of producing offspring from the female he has located.
(Actually it's a bit more complicated than this, but this simplifies
the picture without (IMHO) distorting it) The author calculated that
the critical time to be 3.8 hours, after that a male should reject
a previously mated female. 

    The authors then observed the squirrels mating and observed
that second matings did, in fact, decrease in time. They also 
found that, on average, males would reject a previously mated female
if she had mated 3.82 hours earlier. 

    The authors concluded that, since the behavior of squirrels
closely matched their predictions. And, since their predictions were
formulated based on sperm competition; sperm competition is most
likely the factor determining male acceptance/rejection of mated
females in 13 lined ground squirrels.

REFERENCE

Schwagmeyer and Parker, 1990, Male mate choice as predicted by
sperm competition in thriteen lined ground squirrels, Nature 348:
62 - 64
Subject: squirrels with calculators
Summary: how do squirrels "know" 3.8 = magic number
Keywords: squirrels, calculators, not

    In regards to my previous squirrel post (actually two), the
thought just crossed my mind that some people might get the wrong
idea (or heaven forbid want to ridicule evolution by making a straw
man of what I said) about how male ground squirrels "know" to 
reject previously mated females.

    First off I would like to make it quite clear that the 
squirrels do not need to be trained in math to determine this. They
don't avoid previously mated females after 3.8 hours because they
understand the underlying mathematical model, but because natural
selection favors males who "know" 3.8 is the magic number. Allow
me to elaborate.

    If a male happens upon a female who had mated, oh 
lets say 2.4 hours previously, decides to go looking for a new
mate, (on average) he would sire less offspring than if he would have
waited. Likewise, if a male waits 5 hours after the first mating
for his chance, he will (on average) produce less offspring than had
he wandered off to search for a new mate. However, males who, for
whatever reason, go searching for mates after 3.8 hours will on
average produce more offspring than males who wait any other 
amount of time. And as time goes on their offspring (who "know"
to start searching after 3.8 hours) will come to make up a larger and
larger percentage of the gene pool. Natural selection will favor
males who search for a new mate when the female they find has
mated 3.8 hours or more ago.

    So males don't need to run around with calculators to
figure out how long to wait, the answer has been passed on to
them by their male ancestors who, by chance, hit upon the right
length of time. 

    One last question could be asked. How do males know if and
how long ago the female mated? I don't know the answer to this. Any
thirteen lined squirrel experts out there? It could be any number
of things. Even a rough estimate could be beneficial to the male.

Subject: evidence for evolution (8 - swordfish)
Summary: female preference before male trait
Keywords: female preference, male trait

    In one of my earlier posts in this series, I presented two
(non mutually exclusive) models of sexual selection. Those were
the "good genes" model and the "runaway sexual selection" model.
Well, there is actually a third model out there also (which does
not exclude the others). I'm not aware of any name for it, I'll
just call it the "existing female preference" model. According to
this model, females have a built in preference for a certain type 
of male, even if that type of male does not exist. 

    The paper I summarize here is in the Nov 9, 1990 issue of
Science. In the article, the author claims that, in swordfish, the
female preference for males with swords existed before males had 
swords.
    Within the genus _Xiphophorus_ there are swordless platyfish
and swordtails. The swordless state is considered to be ancestral.
Basolo (the author) experimented with females of the species _X_.
_maculatus_. Males of this species are swordless. He placed a 
female in the center of an aquarium that was sectioned into three
areas. On one side, he placed a normal male. On the other he placed
a male with an artificial sword attached. She noted that the female
prefered (stayed on that side of tank and offered mating displays)
the male with the artificial sword. The experiment was redone and
males switched sides (to control for side bias). The result was the
same, the female prefered the male with the sword to the swordless
male. 

    The author further experimented to determine if it was the
sword itself the female was cueing on. To do this she repeated the
above experiment except in this case both males had artificial
swords. One sword was colored, the other was opaque (clear plastic).
In this case the female prefered the male with the colored sword.
The control (for side preference) was also run. In addition, the
author removed the swords and switched them between males and ran the
tests (and controls) again. The results were once again, the same.
The female prefered the male with the visible sword.

    So, the data she collected were. [small aside, yes the word 
"data" is plural. "Datum" is the singular. Computer types simply
missused the term often enough that it has become accepted in
computer literature]

1.) Females (from this species that had never seen males with swords)
prefered males with swords.

2.) The females were not cueing on some side effect of the sword. (The
clear vs. colored sword showed this. One possible side effect the
female could have cued on was a unique swimming motion induced by
the presence of the sword)

3.) The female (in the colored vs. clear sword experiment) was not cue-
ing on some other trait of the two males. (The switching swords exper-
iment showed this. When the swords were switched, her preference
switched.)

    The author then concluded that the females in this genus have
a pre-existing preference for males with swords. It is not surprising
then that many species in the genus have swords, males have exploited
this bias. What may be surprising to some is that some species don't
have swords. This (IMHO) illustrates a pervasive misunderstanding that
most people (and sadly many biologists) have about evolution. Evolution
is _not_ goal oriented. In this case there is no "selection pressure"
for males to develop swords. They are not being pushed to develop swords.
If, by chance, one males fins by chance happen to be longer than the
other males in his population, he will enjoy greater reproductive
success (because he is more "swordlike" than the others). This _could_
continue until enough mutations have been selected for that males in
this species have swords. But (and this is a very important but) there
is no mechanism that is directing this to happen. In other words, there
is no pressure on the males to develop swords. It's a fairly subtle
point that is hard for many in our culture to accept. We live in a
culture that likes to view things in terms of progress or heading
towards a goal. Evolution is neither progress nor goal oriented.

REFERENCE:

Basolo, 1990, Female preference predates the evolution of the sword
in swordtail fish, Science 250: 808 - 810

Subject: evidence for evolution (10 - intro)
Summary: genetic drift, Mullers ratchet
Keywords: drift, ratchet

     I'll discuss here a paper in a recent issue of
Nature. The author, Lin Chao, examined the RNA virus phi 6 to see if
Muller ratchet was operating. I'll post this in two parts. In part
one I'll explain what Mullers ratchet and genetic drift is. In part 
two I'll summarize the paper and explain it's significance.

    H.J. Muller proposed, in 1964, one reason why sex may be
beneficial to organisms. In a strictly asexual lineage, recombination
is not possible (in sexual lineages it, of course, is). Thus, any
mutation that occurs in an asexual lineage can only be corrected in
one of two manners. The back mutation can occur or a compensating
mutation can occur. Since mutations occur at random, the probability
that the next mutation occuring in the lineage is the back mutation
is low. Thus, each new mutation the lineage absorbs is likely to be
a unique mutation. And, since mutations are most often deleterious;
an asexual lineage is expected to decrease continually in fitness.
Compensating mutations are also highly unlikely. This continual
decrease in fitness, driven by mutations, is called Mullers ratchet.
The term comes from the idea that each mutation moves the "ratchet"
one notch forward and it cannot be moved back.
  
     Sexual lineages
have one other option to overcome mutations, recombination. If a
gene is mutated in a sexual organism, recombination can occur with
it's mate's homologous gene. Thus the offspring will have a non-
mutated gene. If a sexual population has several different mutations
in various genes in it's gene pool; it is possible through recombina-
tion to reconstruct an unmutated progeny. Recombination is several
orders of magnitude more common than mutation, so it can easily
"take care of" mutations as they arise. Some (most?) biologists think
this is why sex evolved (and continues to this day). It eliminates
the operation of Mullers ratchet (because organisms can shuffle all
the "good genes" in the gene pool into one organism).

    In order to understand the paper I will outline in my 2nd
post, one must understand one more concept, genetic drift. I'll
only explain this briefly.

    Genetic drift is caused by a binomial sampling error of the
gene pool. In a finite population (as all biological populations
are) the gametes contributing to the next generation are a sample
of the alleles in the gene pool. As anyone who has any grasp of
statistics can tell you; the smaller a sample, the less likely
you are to get an accurate description of the population. So, in
populations that undergo a bottleneck (a severe reduction in numbers),
the sample of alleles going to the next generation is a small sample
of the population gene pool. Thus, the frequency of each allele in
the following generation will be different in the next generation due
solely to chance (binomial sampling error to be specific). [Note:
this is assuming natural selection is not operating on the allele
in question. Natural selection also changes allele frequencies.] 
The greater the bottleneck, the more severe the sampling error, or
genetic drift, is. [Drift occurs to some degree in all population
whether they are bottlenecked or not. The smaller the population,
the greater effect drift as.] 

    Drift relates to Mullers ratchet in the following manner. When
a mutation occurs in an asexual lineage, only one organism has the
mutation. The rest of the organisms are unmutated. If the mutation is
only slightly deleterious, it can increase via drift and eventually
the unmutated version of the gene can be lossed. When this occurs, the
ratchet has clicked a notch and can't be reversed. (The unmutated gene
is lost from the population barring a back or compensitory mutation)
Of course, to _strictly_ asexual lineages, there is no such thing as
a population. Each organism is it's own species. But, there are
precious few strictly asexual organisms in the world. Most asexual
lineages find some way to "mix and match" genes with those like
them, and those not really all that much like them. So, in that case,
the population of organisms is mean-
ingful.

Subject: evidence for evolution (10 - data)
Summary: Muller ratchet in an RNA virus
Keywords: drift, ratchet

    In this paper Lin Chao propagated 20 lineages of the RNA
virus, phi 6. This virus was chosen for two reasons. One, it is
asexual. (Actually, it has three distict regions that can be re-
combined, but recombination can not occur within these regions.)
And two, it has a mutation rate several orders of magnitude higher
than similar DNA viruses. (In addition, DNA viruses reproduce
sexually.) All 20 lineages derived from a single parent virus.

    In each lineage he subjected the virus to 40 growth cycles.
Each cycle consisted of picking a single virus and growing up a 
population of 8*10^9 viruses from it. So, the virus was subjected
to 40 bottlenecks to intensify drift. If the single virus chosen
contained a mutation, the mutation could not be rectified. The
ratchet had clicked a notch. (Intensifying drift corrected for
the fact that a small amount of recombination is possible in 
this virus as I mentioned before.)

    At the end of the forty cycles he measured the fitness of
each of the 20 lineages (compared to the original parent virus).
(Fitness of each lineage was measured three times.) He found that
each of the 20 lineages differed markedly in fitness. One lineage
increased in fitness by 6%, all others decreased in fitness. One
lineage decreased to 28% of the parents fitness. The average of
the lineages was 78% as fit as the parent (the 95% confidence
interval did not include 1 (fitness of parent virus)).

    The author concluded that the (highly significant/ 
P=0.0001) decrease in fitness was due to Mullers ratchet. Each
lineage continued to absorb mutations it could not repair. Of
course the 6% increase in fitness was an interesting result.
No real satisfying explanation of that was given. (If Mullers
ratchet was assumed to be operating in the past, however, one
possibility immediately springs to mind.)

    The paper is important because Mullers ratchet
looks good on paper, but it had only been demonstrated once
before (in ciliates. Incidentally, allowing them then to have
sex stopped the ratchet.). Given that it is one of major 
reasons sex is thought to have evolved, it's nice to have some
empirical evidence that the phenomena actually exists. 

REFERENCE:

Chao, 1990, Fitness of an RNA virus decreased by Muller's ratchet,
Nature 348: 454 - 455

Subject: evidence for evolution (16-humans)

I just saw a paper concerning human evolution in PNAS (Proceedings
of the National Acedemy of Sciences) and thought I would summarize
it. This bears only tangentially on that discussion.

    The authors of this paper (a bunch of people from Cavilli-
Sforza's lab) set out to draw a phylogeny of 5 human populations and
determine whether the differences in the populations were due to
natural selection or genetic drift. They gathered data
on 100 genetic polymorphisms from people from these 5 groups: two
groups of African pygmies, Europeans, Chinese and Melanesians. A
polymorphism is a trait (in this case a gene sequence) that is
variable in a population. For example, eye color in humans is a
polymorphisms. 

    Phylogenies are drawn by comparing gene sequences and
assuming that sequences more similar to each other are more
closely related than sequences less similar to each other. [For
a brief intro into the theory behind this see Li and Graur, 1991,
_Fundamentals of Molecular Evolution_, Sinauer. There's a little
more to it than I'm letting on. However, phylogeny construction
is (IMHO) so unbearably boring I don't want to get into the details
here.] They arrive at a tree that shows the African populations
branching off from the others about 100,000 years ago. (Estimating
time of divergence assumes a constant rate of mutation - the
relationship of the sequences do not. IMHO, it is not a great idea
to automatically assume mutation rates are constant.) Next the
Melanesian stock split off from the European/Chinese lineage. Then
the Europeans and Chinese split. Finally (in the other half of the
tree) the two African stocks separated.

    This tree, however, has serious problems. I won't get into
them but basically there are a series of checks you can run to see
if the tree the computer spits out is reasonable. This tree wasn't.
For one thing the tree required Europeans to have an incredibly
slow rate of evolution compared to the other populations. The
authors find this unlikely although they add that the population
explosion due to the agricultural revolution may have frozen drift
and slowed evolution in Europeans by 20-25%. 

    Using some historical evidence the authors make the assumption
that the European stock was an admixture of two other lineages. They
then feed the numbers back into the computer and get the following
tree. The first split is again the African/others bifurcation.
Next the Chinese and the Melanesians split off. Then the European
population is formed as a hybrid of the Chinese and as yet undiffer-
entiated African stock. Finally the two African stocks diverge. The
authors conclude this tree is more reasonable.

    Next they tried to determine if the distribution of polymorph-
isms is due to drift or selection. They did this by calculating the
Fst value for each polymorphism. Fst values are a measure of the
variation in a subpopulation with respect to variation in the pooled
population. (For details about Fst see Hartl and Clark, 1989, Principles
of Population Genetics, Sinaeur.) They determined a distribution of
Fst based solely on a model of drift and compared that to the numbers
they calculated. They rejected the null (P=0.0023). There were too
many high and low Fst values (and not enough in the middle, therefore)
to be consistent with drift alone. Extraordinarily high values of
Fst indicate disruptive selection. Very low values indicate stabilizing
selection. 

    So basically the authors constructed a phylogeny of 5 human
groups they felt was reasonable and determined that some of the
differences in the gene pools of these groups was due to natural
selection. I thought the paper was pretty good although sketchy in
some portions. In any case, a reasonable preliminary data set and
interpretation.

REFERENCE: 

Bowcock, et. al., 1991, Drift, admixture and selection in human
evolution: A study with DNA polymorphisms. PNAS 88: 893-843

Subject: evidence for evolution (17-endosymbionts)
Summary: double endosymbionts

    Cholorplasts and mitochondria are organelles within eu-
katyotic cells (cells of organisms other than bacteria, which do
not have organelles). These organelles have their own genetic material.
It has been shown previously that organellar DNA is much more similar
to bacteria than to nuclear DNA from eukaryotes. This, and other
evidence, led scientists to the now widely held belief that
these organelles were once free-living prokaryotic cells that
began living in proto-eukaryotic cells and eventually the two types of 
cells required each others presence for existence. They were
obligate endosymbionts. It's worth noting that organelles
still reproduce autonomously within eukaryotic cells.

    Recently, a paper in Nature provided evidence for a double
endosymbiotic event in cryptomonad algae. Several lines of evidence
led researchers to conclude this double event had taken place. First,
most chloroplasts are double-membraned (one membrane from the proto-
eukaryotic cell, one from the endosymbiont bacteria). Chloroplasts from
cryptomonad algae have more than two membranes. Also, these chloro-
plasts contain what is called a nucleomorph, a DNA containing
structure thought to be the vestige of a eukaryotic nucleus. (Pro-
karyotes and organelles don't have a membrane bound nucleus, their DNA 
just "floats free".) 

    The clincher came when the researchers amplified 
up regions of the 18S rRNA gene (using PCR). They found two different 
length sequences that they called Nu and Nm. Nu they believe to be from
the nuclear DNA of the algae and Nm from the nucleomorph (they are
still trying to get rigorous proof of this.) The two sequences were
very divergent. The Nu was similar to nuclear DNA from amoeboid
protozoans and the Nm sequence is similar to red algae. The authors
conclude that cryptomonad algae is a chimera of two endosymbiotic
events. First a endosymbiotic event in which red alge was formed, 
then this eukaryotic red algae being taken into a protozoan creating
the crytomonad algae. 

REFERENCE:
Douglas, et. al., 1991, Cryptomonad algae are evolutionary chimaeras
of two phylogenetically distinct unicellular eukaryotes, Nature 350:
148-150

Subject: evidence for evolution (9 - fossils)
Summary: some data from the rockhunters
Keywords: fossils
In this one I summarize a couple of paleontological papers. 

    The first paper is a report from Science by Jeram, et. al. In it
they describe fossils of land animals from the Silurian. They found an
arachnid (spider) and two centipedes. The kicker of the paper was that
land was not supposed to be colonized by animals by the Silurian. But,
finding predatory arthropods indicates a stable ecosystem containing
animals much sooner than expected. [Aside to the good guys; isn't it
nice to have a theory that is enriched, rather than embarrased, by
new data] This finding even made it's way to the popular press, my
mom sent me a newspaper clipping.

    The second paper appeared in Nature and was authored by Pil-
beam et. al. In this paper they describe two recently found _Siva-
pithecus_ humeri and they discuss the hypothesis that it was closely
related to the genus _Pongo_. The upshot of the paper is, previous
skull specimens of _Sivapithecus_ indicated that it was probably
closely related to _Pongo_, however, the newly found humeri are
not at all similar to _Pongo_ The authors conclude that the data
is not sufficient to make a descision at this time. 

   There is also an
article about evolution of arthropods in that same issue of Science,
but it's not really that interesting. 

REFERENCES

Jeram, et. al., 1990, Land Animals in the Silurian: Arachnids and 
Myriapods from Shropshire, England, Science 250: 658 - 660

Pilbeam, et. al., 1990, New _Sivapithecus_ humeri from Pakistan and
the relationship of _Sivapithecus_ and _Pongo_, Nature 348: 237 - 238 

Subject: evidence for evolution (11)
Keywords: corn, caterpillars, wasps

    Well, I haven't heard any creationists on this board claim
recently that there is no evidence for evolution, but I'll keep this
series going since all the mail I've got concerning it has been
favorable. I'll summarize here a paper from the most recent issue 
of Science. 

    In this paper, Turlings, et. al. investigate the interactions
of corn plants, caterpillars and parasitic wasps. The wasps parasitize
the caterpillars that, in turn, eat corn. The authors found that corn,
when eaten by caterpillars, releases chemicals (terpenoid volatiles)
that attracts wasps.

    To determine what stimulus caused the release of these
chemicals Turlings tested the following leaf types with respect to
their ability to attract wasps: 1.) leaves that caterpillars had
eaten 2.) leaves that were mechanically damaged (cut w/ razor blade)
3.) leaves with caterpillar saliva on them. Note that the first
type of leaf would have both mechanical damage and caterpillar
saliva on it. It had been previously established that wasps were
attracted by terpenoids.

    The authors found that the first type of leaf (caterpillar 
chewed) attracted the most wasps. They concluded that a combination of
damage and saliva were required to efficiently attract wasps.

    In addition to measuring wasp attraction, they analysed the
chemicals released by the corn by gas chromotography. This was to insure
that terpenoids were indeed being released. They were, so Turlings concluded
it was the terpenoids that was attracting the wasps (and these terpenoids
were only produced in response to caterpillar damage).

    It had previously been shown that plants produce chemicals
to ward off grazers. Most of these chemicals, however, work in a 
straightforward fashion. Bug eats chemical; bug dies. This is one of
the first papers to demonstrate a chemical defense that works in a
more roundabout way. Bug eats plant. Plant releases wasp attracting
chemical. Wasp eats bug. 

    The authors do not discount the possibility that the terpenoids
may also harm the caterpillars in some direct way. But, the primary
value of the terpenoids to the corn is its ability to attract a
predator of the caterpillar. There is more to the paper, but I
just wanted to hit the highlights.

    In the recent Nature there are a couple of very interesting
articles (about wrens). I'll try to get around to summarizing them
this week sometime.

    Aside to Ranjan: I am still preparing my post on the Hardy
Weinberg equilibria; I haven't forgotten.

Chris Colby
email: colby@bu-bio.bu.edu

P.S. If you are wondering what this has to do with evolution ask
yourself this question, how did this system arrive at this point?
Remember Steve Timm claimed that creationists (some? most? all?)
believe that before "the fall" there were no predators.

    It is easy to construct a plausible way for this system
to reach the point it is now at given evolutionary theory. I don't
see how you can given a creationist scenario. Both the corn and wasps 
must change in the interim between the supposed fall and present time.
Creationism provides no mechanism for change.

REFERENCE:

Turlings, et. al., Exploitation of Herbivore-Induced Plant Odors by
Host-Seeking Parasitic Wasps, Science 250: 1251 - 1252

Subject: speciation has been observed
 "Though evolution has been studied for years, scientists have never
observed a single species evolving".  So what?  Evolution has been studied
for just over a hundred years.  Speciation takes *LONGER* than just over
a hundred years.  If you just study evolution for about a hundred years, 
all you would expect to see is microevolution within species, and perhaps
the splitting off of subspecies who might be on the road to speciation.
Scientists *have* observed both of these events.

    Creationists seem to want to define species evolving solely
in terms of speciation. Microevolutionary change doesn't seem to
fit their bill as evolution. In fact I just responded via email
today to some guy who didn't understand how the English moths
had anything to do with evolution. (To be fair, I'm not sure if
he was a creationist or just didn't get my point.) As Kathleen
pointed out, evolution has been observed (microevolutionary
changes and the beginnings of speciation). Most creationists (as
well as many evolutionists, perhaps) would be surprised to know that
speciation _has_ been observed!

    In the genus _Tragopogon_ (a plant genus consisting mostly
of diploids), two new species (_T._ _mirus_ and _T._ _miscellus_)
have evolved. This occured within the past 50-60 years. The new
species are allopolyploid descendents of two separate diploid
parent species. 

    Here's how it happened. The new species were formed when
one diploid species fertilized a different diploid species and
produced a tetraploid offspring. This tetraploid offspring could
not fertilize or be fertilized by either of it's two parent
species types. It is reproductively isolated, the definition of
a species (well, the most common definition, at least.) The
paper I have corresponding to this are great. One new species,
_T._ _mirus_ has arizen at least three separate times. 

    So, speciation _has_ been observed in case they bring up
that again. In fact, it happened instantly in this case. Plants
are amazingly plastic in regards to genetics, so it really isn't
all that surprizing that the first (as far as I know) observed
speciation event would be something like this in plants.

Chris Colby
email: colby@bu-bio.bu.edu

REFERENCES:

Soltis and Soltis, 1989, [the title is mangled on my photocopy],
Amer. J. Bot. 76(8): 1119 - 1124

Roose and Gottlieb, 1976, Genetic and Biochemical Consequences
of Polyploidy in _Tragopogon_, Evolution 30: 818 - 830

(The Soltis paper looks at chlorplast DNA, the Roose paper
examines allozyme data. Both are, IMHO, fairly decent papers.)

Subject: evidence for evolution (12 - exon shuffling)
Summary: nothing like "The Curly Shuffle"
Keywords: exon, shuffle, intro

    I've mentioned the term exon shuffling in several of my
posts, so I might as well get around to explaining what the hell 
I'm talking about. This is especially true since there is a paper
in this weeks Science about the "Exon Universe" that will be the
second part of this article. In this introduction to the paper,
I'll explain a little about gene structure and what exon shuffling
is. (Keep in mind that DNA codes for RNA which codes for protein)

    The bacteria E. Coli was used in most of the very first
molecular genetics experiments. When the first genes were sequenced
from it, it was found that all the information for the protein
lay in one continous stretch (an open reading frame (ORF)). It
came as a bit of a surprise when the first eukaryotic genes were
sequenced and this was not the case. It seemed typical eukaryotic
genes contained several open reading frames of DNA interrupted by
sequences of DNA that did not code for anything. The coding regions
were dubbed exons and the intervening sequences were dubbed introns.

    It was soon found out that exons commonly coded for a
functional domain or subunit of a protein. In other words, that
introns often separated useful "building blocks" of proteins. Of
course this led to speculation that, perhaps exons could be
duplicated, deleted or "mixed and matched" from an existing gene
to create a whole new gene with a new function. If a whole gene
was duplicated for instance (this is fairly common), one gene
could continue doing its job while the other is free to evolve a
new function by swapping exons with other duplicated genes. This
is what exon shuffling refers to.

    Of course, this would be a great way to gain new useful
genes and their corresponding proteins in a hurry. And, it wasn't
too long before exon shuffling was confirmed to have happened.
Two genes, low density lipoprotein (LDL) receptor gene and the
epidermal growth factor (EGF) were shown to be mosaic genes. Al-
though they were functionally unrelated, they shared a few common
exons. 

    It may seem a bit farfetched to those who don't know much
about molecular genetics that exons could just whiz all over the
genome and conveniently plunk down in a useful place. In fact there
are plenty of mechanisms for moving DNA from one part of the genome
to another. I'll mention a couple. 

    One is gene conversion. This is a phenomana by which one
stretch of DNA "erases" another stretch and copies itself in it's
place. The mechanism is well known, but I don't have time to
explain it. Any molecular bio text will have that info.

    Another is transposition. This is when a stretch of DNA 
simply excises itself from one part of genome and moves itself
to another. Transposons are pieces of DNA that do this. Many
biologists (including myself) tend to think of them as molecular
parasites. They don't do any good to the cell or organism. But
since they move around the genome so much, it's hard to get rid
of them. Transposons carry a few genes with them, usually only the
genes required for their own movement.

    If two transposons surround a stretch of DNA, they can
carry that stretch of DNA along next time they both move if they 
move as one big unit.

    These processes aren't directed or cognizant in any way, so
an exon doesn't know to get shuffled to the right place. In fact,
often an exon (or transposon) will plop down in the middle of a
functional gene. The result is one dead organism. But, occasionally
a good rearrangement will take place. It's a hit or miss phenomena.

    So, theres an explanation of exon shuffling and a bit of
info as to how it could happen. Tomorrow, I'll try to post a
summary of the paper in Science.

Subject: evidence for evolution (12 - data)
Keywords: exon, shuffle, intro

    The paper is called "How Big is the Universe of Exons". Recall
that an exon typically encodes on functional domain of a protein (for
example a DNA binding domain). Duplicate genes can "swap" introns
and quickly evolve new proteins. A homologous DNA binding exon, for 
example, might be found in many entirely unrelated gene, indicating 
it was imported intact from another gene. This "prefab" construc-
tion of genes is called exon shuffling.

    The authors of the paper made the following assumption in
the beginning of the study. Since introns (the sequences that in-
tersperse between exons) are found in all eukaryote taxa _and_
they typically are in the same place in homologous proteins, the
intron/exon structure of genes must be ancestral. The competeing
point of view is that introns are rather new and spread through
all taxa as transposon-like elements. Some intron placement lends
credence to this view, but, IMHO, most introns were probably
present in the progeonote (latest common ancestor to all living
organisms). Some introns invaded later. As an aside I will mention
that bacteria do not contain introns, some biologists take this to
mean that they "dropped" their introns to streamline their genomes.
Others take this as proof that introns invaded after the divergence
of prokaryotes and eukaryotes. For what it's worth, I favor the
first hypothesis. 

    The authors then set out to calculate how many exons would
it take to account for all the proteins we have in all organisms
today. This assumes modern day proteins did not each evolve slowly
but were assembled by throwing togethor domains until something
worked.

    To do this they plugged their computer into the Genbank and
EMBL databases and basically looked at every gene ever sequenced
(a bit of an exaggeration). They then went through and narrowed the
list of sequences down to non-homologous genes and non-homologous
sequences within genes. For example, if the alchol dehydrogenase
sequence from one species was used, the sequences from other
species were thrown out. Likewise, if a gene had more than one
domain that was identical (not uncommon) the "extra" domains were
deleted. All this was done in an attempt to eliminate duplicate
exons from known homologous sources. (Note: all sequences were
first "transcribed" from DNA sequences to amino acid sequences
via the universal genetic code - this was done by computer)

    Much mathmatical/statistical/computer simulation mayhem
followed 8-) I'll supply the reference for those who want to wade
through the gory details. (I'm still mulling over some of the
analysis) Basically, however, what they did can be explained as
followed. From the sample of genes they took out of the database,
they made pairwise comparisons and checked how many identical exons
they had. They used this sample number as an estimate of the total
of identical exons in the population (all organisms). They concluded
that between 1000 and 7000 exons were needed to create all the
proteins we see today. A rather small number, all things considered.
 I think I almost broke my wrist 8-)
At least now I understand the appeal of creationism ;-) )

    At the end of the paper a considerable amount of time is
spent examining all the possible assumptions and consequent errors
that could be included in the study. They are rather numerous, but
the authors do their best to deal with them. They range from the
chances of forming two identical exons by chance to homologous
exons diverging in amino acid sequence, but not function. Some
problems would cause the estimate of total exons too small, others
would cause the number to be too large.

REFERENCE:
Dorit et. al., 1990, How Big is the Universe of Exons, Science 250:
1377 - 1382

Subject: evidence for evolution (13 - introns)
Summary: introns of ancient origins
Keywords: introns, chloroplasts, cyanobacteria

    This is number 13 in my series of postings about current
research in evolution. I'll summarize two papers from a recent
issue of Science, both of which basically reported the same 
finding. I'm kind of pressed for time today, so this will be a
bare bones summary. But, as always, I'll supply the references.

    First a bit of background. In eukaryotes, (basically all
organisms except bacteria) genes typically are not found as
a single uninterrupted reading frame. There are sequences inter-
spersed within the coding region of genes. They are excised
after the DNA is translated into RNA. These excised DNA sequences
are called introns (the coding DNA sequences are called exons).

    In the two papers I will summarize, the authors present
evidence of an ancient origin for introns. 

    According to the endosymbiotic hypothesis of eukaryote
evolution, modern day chloroplasts are the descendents of ancient
cyanobacteria. These cyanobacteria were engulfed by an ancient
cell and a symbiotic relationship was established such that the
cyanobacteria simply continued to live inside the engulfing cell.
There are also free living cyanobacteria alive today. The authors
of the papers document the presence of an intron in a gene of
both modern day cyanobacteria and chloroplasts. In both cases
this intron is the same type in all the genes looked at (it is
a group I intron) and it is also in the same position. They
argue that this implies the intron was present in the gene before
ancient cyanobacteria split into its two present day lineages
(modern cyanobacteria and chloroplasts).

    In the first paper the authors document a group I intron
in the same position in the leucine tRNA gene in two species of
_Anabena_ (cyanobacteria) and in the chloroplasts of several land
plants (bean, liverwort, maize, rice and tobacco). In the
second paper the authors (a different bunch of fellows) show
a group I intron in the leucine tRNA gene in five species of
cyanobacteria and many chloroplasts from very different plants

    From these data the authors (in both papers) argue that this
is evidence for the intron predating the split of modern cyanobact-
eria and chloroplasts. If the common ancestor of these two groups
(ancient cyanobacteria) had this intron in that position, it's
current distribution can be explained by simple inheritance; both
lineages retained it. The alternate explanation would be that the
intron invaded all these lineages. Group I introns are mobile in
some lineages; they can excise themselves from one stretch of DNA
and insert themselves in another. However, it is highly unlikely
that the same type of intron would plunk down in the same spot in
all these genes. The first hypothesis (the intron was in the 
common ancestor) is, IMHO, much more likely. 


REFERENCES:

Xu, et. al., Bacterial Origin of a Chloroplast Intron: Conserved
Self-Splicing Group I Introns in Cyanobacteria, Science 250: 1566
- 1569

Kuhsel, et. al., An Ancient Group I Intron Shared by Eubacteria
and Chloroplasts, Science 250: 1570 - 1572

Subject: evidence for evolution (14 - sex ratios)

    This is part 14 in my series called "evidence for evolution".
I'll explain what this is about. In this series
I post summaries of recent scientific papers about evolution. I
choose the papers from mainstream, peer reviewed scientific
journals (not _Evolution_ or _Journal of Molecular Evolution_ or
any of those journals). This is to demonstrate that evolutionary
biologists meet the criteria of scientific worth as judged by
scientists in other fields. (As an aside, _Nature_ publishes
about one to two evolution papers per week. I have never seen
a creationist paper presented there.) No single post is meant
to be a capsule proof of evolution. Each is merely more evidence 
that it did, and does, occur. In addition, I have been chosing
papers that have come out recently. This is not a compendium of
classic papers, but rather stuff on the cutting edge.

    I'll summarize here a paper that demonstrates evolution
occuring in a laboratory situation. It appeared in a recent
issue of _Science_(1).

    In almost all dioecious species (species with two sexes),
the sex ratio is 0.5. There are 1/2 males and 1/2 females. In most
species,the Mendelian rules of inheritance explain mechanistically
why this is so. For example, in humans the offspring from any one
mating has a 50 percent chance of being male or female. This is
because the male sperm has a 50 percent chance of contianing a
Y chromosome and a 50 percent chance of containing an X chromo-
some. Female eggs only contain X chromosomes. Individuals that
are XX are female, individuals that are XY are male. Given any
initial sex ratio, the next generations sex ratio will be 0.5.
(the proof is left as an exercise to the reader) The only ex-
ception to this would be a sex ratio of 1 or 0. An all male or
all female population has no hope of regaining a balanced sex
ratio. 

    The question can be asked, is the sex ratio then just a
non-adaptive consequence of the independent assortment of X and Y
chromosomes in male sperm? Or, is the ratio adaptive and Mendel-
ian assortment an adaptive trait that has evolved?

    The authors of a recent paper put this to the test by
studying the Atlantic silverside fish _Menidia_ _menidia_. This
fish has an unusual life cycle in that, during the early months
of the year mostly female offspring are produced. In the
summer months mostly males are produced. The bias in the sex of
the offspring is induced by the water temperature. Female offspring
are produced while the water is cold, males while it is warm.
The sex ratio across the whole year balances out to 0.5. This
sex bias is caused by temperature dependent sex determination,
_not_ temperature dependent sex mortality. In other words cold
water makes baby female fish form, it doesn't kill male baby
fish. The same embryo could be male or female depending on
the temperature it is raised at (i.e. Mendelian segregation does
not influece the sex ratio in this species.)

    The authors captured hundreds of these fish and maintained
them in aquaria for five to six years. Some aquaria were maintained
at low temperatures, others at high temperatures. In the low temp
aquaria, the populations began with mostly females. The sex ratio
, for example, in one low temp tank was 0.70 (70% female) In the high
temperature aquaria, the populations began with mostly males. In 
one of the low tanks the sex ratio was 0.18. Both of these, given
the population sizes, are significantly different than 0.50.

    As the experiment progressed, the sex ratios changed
from the highly skewed initial conditions. In all the populations
the sex ratios converged on 0.5. The trajectory of the sex
ratios converging on 0.5 differed between many of the tanks. 
In one tank, the next and all subsequent generations were at an
0.5 sex ration. In another, it slowly converged upon 0.5. In
yet another it reached 0.5, then overshot slightly, then 
returned. This indicates that a sex ratio of 0.5 is somehow
adaptive (there is a lot of theory as to why this may be - I
may bore you with it later some time) because the fish evolved
from a skewed ratio to a balanced ratio. Since chromosome
assortment does not determine sex in these fish (temp does),
the only explanation for their convergence to 0.5 is natural
selection favored fish that produced an abnormal amount of
the minority sex. (If males are lacking, any fish that produces
male fish will contribute more than average to the gene pool).
This is a frequency-dependent kind of selection. As the sex ratio
approaches 0.5, fish who produce a disproportionate amount of
either sex will contribute less than average to the gene pool. 

    Finally, notice that evolution has occured. The experiment
started with populations of fish that produced skewed sex ratios
and ended with populations that produced balanced sex rations.
Since the environment was held constant, the change in the pop-
ulations was therefore genetic. In other words, the gene pool
changed over time. This is the definition of evolution.

    Of course, the authors were mainly concerned with the
result of sex ratios apparently being adaptive and did not
make much ado about evolution being shown to occur (for much
the same reason that modern astronomers don't constantly
stress, or try to prove, the earth is round). This is only
one of many papers actually demonstrating evolution in the lab.
There are also many demonstrating evolution occuring in the 
wild (any evolution text can provide these refs - or email me
if you are interested). Also, as I have posted before, speciation
has also been documented to occur (I'll supply these refs (2, 3))

REFERENCES:

(1) Conover and Voorhees, 1990, Evolution of a Balanced Sex Ratio
by Frequency-Dependent Selection in a Fish, Science 250: 1556 - 1558

(2) Roose and Gottlieb, 1976, Genetic and Biochemical Consequences
of Polyploidy in _Tragopogon_, Evolution 30: 818 - 830

(3) Soltis and Soltis, 1989, [ title mangled on my photcopy 8-( ]
Amer. J. Bot. 76(8): 1119 - 1124

Subject: evidence for evolution (15 - crossbills)
 Here's a look at what a couple
of biologists have been up to recently.

    A lot of "armchair evolutionary" explanations of complex
traits follow the "little trait becomes a big trait" mode. In other
words the complex trait begins as a barely functional abnormality
and is gradually shaped by selection into a fully functional bit
of morphology (or behavior or biochemistry). These "just so" stories
are usually, however, completely unsupported by data (but, they aren't
refuted either).

    The authors in the paper I'll summarize briefly here add some
weight to one "little trait becomes a big trait" explanation. Benkman
and Lindholm studied the red crossbill (_Loxia_ _curvirostra_) to
examine how this birds strange bill evolved. The crossbill, as it's
name implies, has a crossed bill. The lower bill curves to one side
and the upper bill curves to the other. The unusual bill shape helps
these birds extract seeds from pine cones.

    Bird bills, like human toenails, can be clipped without
injuring the organism. And, again like toenails, they grow back.
The authors used nail clippers to trim the beaks of the birds
in such a way that they were not crossed. It took about 36 days
for the bills to grow back from an uncrossed state to a crossed
state. The authors used this bill growth to mirror the probable
phylogenetic change from uncrossed to crossbilled birds.

    The authors first separated the birds into a control and
an experimental group. They then measured how long it took the
birds in each group to extract seeds from a cone. Both groups
were statistically the same. They then clipped the beaks of the
experimental group and measured, over a 36 day period, how long
it took each group to removed seeds from a cone. As you would expect,
the control group did not change throughout the experiment since
it remained unaltered. The experimental group, however, did change.
In the first day after clipping it took an average of 5.28 seconds
for a bird to get at a seed. This was up from 1.34 seconds prior to
clipping. As the experiment went on, the birds got better and
better until at 36 days it took them only 1.68 seconds to get
a seed (statistically not significantly different from 1.34).
This increase in seed gathering seed was interpreted as a function
of bill crossing. The authors concluded that the crossbill trait
was selected every step of the way from an uncrossed ancestor,
because as the bill became more and more crossed, the birds
ability to quickly secure food increased. They also noted that
slight bill crossings have been sighted in straight billed
species of birds.

    John Krebs (in the accompaning "News and Views" article)
notes that the paper does not address the changes in musculature,
tongue morphology and behavior that must accompany the change
in bill morphology. But, he notes that these birds provide a
very interesting avenue with which to pursue questions of this
type.

    Well, there you have it. A short "gee-whiz" paper from
Nature. I sort of liked it (it had a good beat and I could dance
to it). Usually I don't buy these "little trait becomes big trait"
arguments, but in this case at least there is a little data to
back up the claim. (I should point out, before Larry accuses me
of being a saltationist ;-), that I'm not implying that complex traits
appear fullblown in "hopeful monsters". I just I think that it is
often the case that the current utility of a trait has little or
nothing to do with it's ancestral utility. Many complex traits may
be exaptations, not adaptations.)

REFERENCE:

Benkman and Lindholm, 1991, The advantages and evolution of a
morhological novelty, Nature 349: 519-521

Subject: evidence for evolution (18 - mimics)
Summary: classic textbook example trashed
Keywords: oops

    Ted, in his own charming way, has explained that all science
is bogus because it is based on false assumptions and that scien-
tists are so caught up in the momentum of what they are doing, they
can't go back and correct their "errors" (apparently this would
involve forgetting mathematics and selectively reading old manu-
scripts). In any case, what gets done can't be undone (ITHO). This brings
me to a recent paper in Nature. First, a little bit of ecology/evol-
utionary theory.

    Mimicry is the phenomena of two (or more) species looking/sound
-ing/smelling/whatever like each other. There are two types of mimicry:
Batesian and Mullerian (should be an umlaut over the u). 

    Batesian
mimicry is when one species evolves to mimic a second species that
has some trait that makes it undesirable to predators. For instance,
a butterfly that tastes good, but mimics a butterfly that tastes
bad, may evade predation as long as bad tasting butterflies outnumber
good tasting ones (it's a frequency dependent kind of thing). The
palatable species benefits because it gains the reward of looking
like a bad tasting species, but it doesn't pay the price; chemical
toxins are costly for an animal to produce. If the palatible species
becomes too numerous, the unpalatible species may suffer as
predators may learn that organisms that have that pattern/color-
ing/sound/smell are O.K. to eat.

    Mullerian mimicry is when two (or more) foul species evolve 
to look/sound/smell/whatever like each other. They both/all benefit
because predators have only to learn one signal to discriminate species
to avoid, instead of having to learn separate cues for each foul 
species. This is a benefit to the prey (only coincidentally a benefit
to the predator) especially if the two (or more) mimetic species occur
at low densities. 

    One of the classic example of Batesian mimicry has been
the viceroy butterfly. Biology texts explain that this butterfly
is a palatable mimic of two species of noxious butterflies, the
monarch and the queen. A new paper in Nature suggests that the
viceroy tastes every bit as bad as monarchs and worse than
queen butterflies. The authors conclude that the mimicry is a
three way Mullerian mimicry instead of the viceroy being a Batesian
mimic to the two Mullerian mimics, the monarch and queen.

    Their experiments consisted of capturing 16 red winged
blackbirds from nature and offering them butterfly abdomens and
recording the response. Only abdomens were offered so that the
bird could not tell species apart by subtle changes in wing
color or morphology. Each bird was offered 8 viceroy, 8 monarch
and 8 queen butterfly abdomens dispersed at random between 24
palatible control abdomens. The percentage of each abdomen type
eaten was recorded as well as mean manipulation time and a
mean response score. The response score was basically an
arbitrary scale ranging from the bird ignoring the abdomen (0),
through pecking once (1), partially eaten (2) to completely 
eaten (3). The results were as follows:

    98% of the control abdomens were consumed by the birds,
68% of the queen, 41% of the viceroy and 46% of the monarch.
The monarch and viceroy scores did not differ significantly;
the other two classes did.

    Mean manipulation time for the control abdomens was
5.3 seconds. For the other species it was: queen = 17.5 s,
viceroy = 23.5 s and monarch = 31.3 s. The monarch and viceroy
were again not significantly different. In addition the viceroy
was not significantly different than the queen. The monarch
and queens did, however, differ significantly.

    Finally, the mean response score for the controls was
2.98. The queen, viceroy and monarchs scored 2.50, 1.98 and
2.10, respectively. In this case the viceroy and the monarch
were the only two classes that did not differ significantly.

    So, all three species were significantly less palatable
than the controls. And, in two of three measures the viceroy
and monarchs were (as a class) less palatable than the queen.
This shows that the classic example of Batesian mimicry is
actually a case of Mullerian mimicry. It also disproves Ted's
notion that once science gets done, it cannot get undone.

    This is my favorite kind of science paper, one in which
something widely held is demonstrated to be just plain wrong.

REFERENCE:
Ritland and Brower, 1991, The viceroy butterfly is not a batesian
mimic, Nature 350: 497- 498

Postscript:
Batesian and Mullerian mimicry involve interspecific interactions.
Intraspecific (within a species) Batesian mimicry has also been
documented. Monarchs obtain their toxins by sequestering cardiac
glycosides of their host-plant, the milkweed. In large flocks(?) of
monarchs there are many that have not spent the energy to sequester
these glycosides; they are getting a "free ride". These monarchs
can then invest more energy towards raising offspring than the
monarchs who "play fair" and spend energy to harbor the poisons.

Subject: evidence for evolution (2 - intro)
Summary: intro to speciation theory
Keywords: speciation, isolation

    This is part two in my series of postings on studies of an
evolutionary nature. As I said in part one, I have two goals in for
this series. One, to show that evolution is an accepted branch of
mainstream science. And two, that contrary to the continual assertions
of creationists, there is an overwhelming amount of data in favor of
the theory of evolution. Again, note that no single post is intended as
a stand alone proof. This post is divided into two section, an intro-
duction (the part you are reading) to provide a bit of background, and
the actual summary of the paper discussed.

    Speciation occurs when two (or more possibly) subsets of a
formerly interbreeding population become reproductively isolated. 
For many years, speciation theoratists thought that virtually all
speciation occured when the two subsets of the population where
separated by geographical boundries. (ie, the species became split
by a river, mountain range or a small group migrated out of the
main region inhabited by the species.) Reproductive isolation foll-
owed physical isolation as the two, now separate lineages, diverged.
This could occur for many reasons, for example mating rituals grew
different or chromosome numbers changed etc. etc. In any case the
end result would be that the two lineages could no longer interbreed
if they encountered each other. (Incidentally this type of specia-
tion is called allopatric speciation).

    A second type of speciation, sympatric speciation, occurs when
two lineages of a formerly interbreeding population diverge to the
point of reproductive isolation while still residing in the same locale.
This was first demonstrated to occur by Guy Bush working on the Apple
maggot fly _Rhagoletis_ _Pomenella_.

    The paper I will outline here is one found in the August 9,
1990 issue of Nature. I will continue this discussion in my next post.

Subject: evidence for evolution (3 - intro)
Summary: basics of sexual selection
Keywords: sexual selection

This is part three in my series of postings. In this post I describe
a paper presented in the July 12, 1990 issue of Nature dealing with
sexual selection in katydids (an insect). I am going to break this
up into two articles, one to outline the underlying theory and ano-
ther to describe the experiment.


    The paper I will outline deals with sexual selection. It is
well accepted that the most intense competition an organism faces is
with members of its own species. Many species tend to have limited diets
and habitat requirements, and an organism must compete with members
of his own species to secure these neccesities. Of primary importance,
however, is procuring a mate. If an organism fails to do that it's
genes are eliminated from the gene pool. (Note that in nature there is
never enough food, habitat and/or mates to go around. There are always
more offspring produced in a population than will be able to reproduce.)

    In many (if not most) animal systems, females choose the males
they wish to mate with. Conversely, males compete for access to fe-
males. For example many male birds defend a territory in order to att-
ract females. In many mammals (ie sheep) the males (rams) engage in
contests to determine which male gets to mate. Obviously the female
will choose the male who wins becuase her sons will then have the genes
for winning these contests and females will choose them. [as a sidenote
this kind of "logic" on the part of females can lead to what is called
"runaway sexual selection". This occurs when the traits favored by sex-
ual selection become linked with the genes for preference of that trait.
This can often push the system in such a way that traits with a lower
survival value are favored because their sexual attractiveness outweighs
their negative survival value. The tail of the male peacock is an oft-
cited example of this - but that's another story].

    But why should females be the one's who choose? Why don't
females compete for access to males? To answer this question, Darwin
speculated that the sex that contributed more energy to the production
of the offspring would be the sex that would be able to exercise pre-
ference. His theory of sexual selection was later expanded upon by
Williams and Trivers.


    In most animal systems it is clearly the female who devotes
the most energy to the production of offspring. The female gamete
(egg) is many times larger than the male gamete (sperm). In addition,
in mammals, females must carry the offspring until birth. And further-
more females of many species provide the lions share of parental
investment after the offspring has been born.

    In the paper I will present in the next article the
authors experimentally test the hypothesis that the sex devoting the
most energy to the production of offspring will be the sex that exerts
a choice amongst mates.

Subject: evidence for evolution (3 - data)
Summary: experimental reversal of parental investment
Keywords: spermatophore, sexual selection

    In their paper, the authors (Gwynne and Simmons, 1990) exper-
iment on a katydid of, as yet, unnamed species and genus. This species
of katydid was observed to be highly variable in male contribution
to parental investment. In these insects, the males transfers a sperm-
atophore to the female after copulation. The spermatophore contains
the ampulla, which contains the sperm, and the spermatophylax, which
the female eats. The spermatophylax has been demonstrated to increase
both the number and fitness of offspring sired by the male (it is a
source of nutrition to the female).

    In their experiment the authors set up two cages. In cage one
(the control) the katydids were allowed to feed on the pollen of their
host plants. In cage two the katydids were allowed to feed on the 
pollen, but were also provided a nutritional supplement (the experiment-
al cage). Therefore, in the control cage (with limited food) the 
value of the males spermatophore is much greater to the female. Females
were introduced to both cages and their behavior was observed.


    In the control cage (with limited food) the males exerted a
mating preference and females competed for mating opportunities
with males. This is because, with a scarcity of food, the male sperm-
atophore became a valuable asset.

     In the experimental cage, the females exerted the
mating preference because with an abundance of food, the male sperm-
atophore was not such a valuable asset. In this way the authors
showed that (in katydids at least) the parental investment is the
determining factor in courtship roles (i.e. which sex exerts the 
mating preference)

REFERENCE

Gwynne and Simmons, 1990, Experimental reversal of courtship roles
in an insect, Nature 346: 172 - 174

Subject: evidence for evolution (4-whales w/feet)
Summary: whale found with legs
Keywords: fossil, whale, feet

    This is my fourth posting in my "evidence for evolution" series.
This will be a short one. It's a short, gee-whiz paper from Science. In
my next post (tommorow, maybe) I'll explain a paper in Nature in which
the authors sequenced DNA from a 17-20 MY old magnolia leaf. I'll tell
what they found (it's cool) and how they did it (also cool). 

    In the July 13, 1990 issue of science, Gingerich et. al. report
on an interesting fossil found in Egypt. It is a whale with feet. The
skeleton is of the species _Basilosaurus_ _isis_. This whale lived in
the Eocene period (in Egypt (then under water obviously)).

     Current cetacea (whales), as you are no doubt aware, do not have
external hind limbs. But whales, which are mammals, evolved from terr-
estrial mammals. This fossil, therefore, is a link between the two. The
skeleton they show is long (16 m) and serpentine. The authors believe
this whale hunted in shallow mangrove or seagrass habitat. It's hind
limb has a short femur and a slightly shorter fibula and tibia. It
has no thumb and a greatly reduced second digit. The other three fing-
ers are quite long (relatively). In short, another variation of the
basic mammalian leg.

    The authors speculate that the limbs were tucked in close to
the body while the whale was swimming (and the topography of the
bones suggest that they are correct). Furthermore, they go on to
speculate that the limbs served as a copulatory guide for the whale.

    The one thing I didn't like about the paper was a lack of
actual photographs of the specimen. They gave graphs and schematic
diagrams of all the salient features, but no photos. I would think
that in a paper of this nature, a picture would have been worth a
thousand words. Maybe they are working on the reconstruction and
want to complete it before display. 

REFERENCE:

Gingerich, et. el., 1990, Hind Limbs of Eocene _Basilosaurus_: Evidence
of Feet in Whales, Science 249: 154-156

Subject: evidence for evolution (5-intro-PCR)
Summary: intro to polymerase chain reaction
Keywords: PCR, amplification, Taq polymerase

    This is my fifth posting in my "evidence for evolution" series.
In this post I will explain a paper in the April 12, 1990 issue of Nature
in which the authors sequence a 17-20 million (yes, thats million) year
old DNA sequence from the chloroplast of a fossilized Magnolia plant.
I will use this post to make two points (besides the usual). One, to
explain the significance of their actual results. And two, to introduce
you to a new molecular biological technique that has opened up a vast
horizon of possible molecular evolutionary studies. The technique is 
called polymerase chain reaction (or PCR for short). This first article
describes the technique. The second article will describe it's applica-
tion. This article assumes some knowledge of basic molecular biology.
I give a reference for a more detailed discussion near the end.

    PCR is a technique that allows a researcher to pick a region
of DNA from a very small sample and amplify it to some usable quantity.
It works by iterating cycles in which only the region of interest is
amplified.

    At the beginning of a cycle the DNA is double stranded (I'll
call the strands the + and - strands). The DNA is then heated and the
strands come apart. Then the DNA is cooled. As it cools, primers bind
the DNA. These primers are short oligonucleotides chosen by the exper-
imentor and added to the DNA mixture at the beginning. They flank
the region to be amplified. One binds to the + strand and the other
binds to the - strand. Their 3' ends both face the region to be amp-
lified (remember DNA is synthesized in the 5' to 3' direction) so that
polymerization can only occur in that region. A DNA polymerase then
begins adding nucleotides to the 3' end of both primers, sythesizing
a new - and + strand of the region of interest. Next, the reaction mix,
(which includes the DNA sample, the primers, single nucleotides and the
polymerase) is again heated and then cooled. This is repeated many times.

    The result is the following. In the first cycle the + and -
strand serve as a template and a new - and + (respectively) copy of
the area of interest is made. When the cycle is repeated the primers
now have more sites to bind to, the original sample DNA sites and
the newly synthesized DNA sites. As the cycles continue, the number
of possible primer binding sites doubles each time. Therefore in a 
short amount of time a negligible amount of DNA can be amplified to
a workable quantity. This is because the amount of templates is
geometrically increasing each cycle.

    This is extremely hard to portray in words. A diagram of this
technique makes things crystal clear. Many biologists I know, including
myself, when first exposed to the idea of PCR said, "Why the hell didn't
I think of that?". It is a very powerful and elegant technique. For a
good, accessable overview (with the pictures to ram the idea home) see
the April, 1990 issue of Scientific American (p 56, The Unusual Origin
of the Polymerase Chain Reaction).

    One further thing is worth mentioning. When you heat the DNA,
everything else in the reaction mix is going to be heated along with it.
At the temperature DNA denatures (strands separate) proteins from most
organisms (like DNA polymerases) also come apart. This presents a prob-
lem. Either the researcher would have to add new polymerase each cycle,
or a heat stable polymerase would have to be found. In fact, a heat
stable polymerase has been found and is used for PCR. The polymerase
is called Taq polymerase. It is call Taq because it comes from the
organism _Thermus_ _aquaticus_, a bacteria that lives in thermal
vents in the ocean. Since the organism lives in water averaging close
to boiling, it's DNA polymerase is stable at these high temps. And,
therefore the Taq polymerase can be added to the reaction mix at the
beginning and will remain active throughout all the cycles. 

Subject: evidence for evolution (5 - data)
Summary: DNA sequenced from 17-20 MY old magnolia
Keywords: magnolia, DNA, sequence, gee-whiz

    In the paper I explain here, the authors (Golenberg et. al.,
1990) sequenced an 820 bp region (the rbcL gene) from the chloroplast
DNA of a compression fossil of a magnolia.

[A brief explanation of chloroplasts (and their DNA): 
    Chloroplasts are organelles found in the cells of plants. They
are the site of photosynthesis. These organelles are autonomously
replicating (i.e. there replication is _not_ tied to the cell cycle.)
They contain their own genome, a single, circular "chromosome". DNA
sequences of their "genomes" and their autonomous nature led Lynn
Margulis to speculate that chloroplasts were once free living organ-
isms that later became endosymbionts in other cells. She also thinks
this explains the presence of mitochondrian in cells (as well as
basal bodies). This is now generally accepted.

    The fossil leaf they extracted the DNA was from a compression
fossil formed when the leaf sank to the bottom of a lake. The con-
ditions were very anoxic (lacking in oxygen) and as a result the
fossil was in very good condition. In the News and Views section of
the same journal they show a photo of the fossil; the leaf was still 
green! And, as you will see, it still contained DNA. They authors 
mention that many well preserved compression fossils were recovered.
These fossils were from organisms living in the Miocene, 17 - 20
million years ago!

    Anyway, the authors extracted what DNA they could from the
fossil and amplified the rbcL gene via PCR. The primers they used
were 30 bp oligonucleotides sythesized to match the sequence of
_Zea_ _Mays_ (corn). Since rbcL codes for a neccesary protein,
ribulose-1,5-bisphosphate carboxylase, they expected the sequence to
be conserved enough for the primers to bind. It was. They also ran some
tests to insure the sequence they got was actually from the fossil
and not an outside contaminant. It was.

    The sequence of the fossil and two extant species of magnolia
are given along with one other plant species. The fossil magnolia,
given the species name _Magnolia_ _latahensis_, yeilded a sequence
similar, but distinct from the extant species of magnolia. The 
magnolia sequences (fossil and extant) formed a cluster distinct from
sequences of closely related species (tulips and petunias for example).
    
    The authors conclude that the sequence they got was from the
fossil and that the fossil was from a now extinct species of Magnolia.

    The power of this technique (PCR) suggests many applications
for evolutionary biologists. Any organism in which the tissue is in-
tact can potentially yield enough DNA to sequence. (This includes
insects in amber, wooly mammoths and musuem specimens) This knowledge
can be used to resolve phylogenies of extinct organisms. Also, if 
enough samples are available, one could estimate the genetic diversity
of past populations of organisms and how it changed through time. 
There has already been a paper of this nature in Jounal of Molecular
Evolution. In that paper the researcher traced the genetic diversity
of Kangaroo Rats of California. Someone in my lab is doing the same
thing on an endangered species of beetle here in Massachusetts. She
is getting the DNA from pinned museum specimens that go back over
one hundred years.

REFERENCE:


Golenberg, et.al., 1990, Chloroplast DNA sequence from a Miocene
_Magnolia_ species, Nature 344: 656 - 658

Subject: evidence for evolution (2 - data)
Summary: isolation mediated by microorganisms
Keywords: haplodiploid, tetracycline, microorganisms

    In the paper outlined here (Breeuwer and Werren, 1990) the 
authors examine two species of wasps living sympatrically (in the
same area).

    Wasps (like ants, bees and termites) are haplodiploid
organisms. In these organisms, females develop from fertilized eggs
(so there is a male and a female contribution to the genome (i.e.
sperm and egg)) while males develop from unfertilized eggs (so there
is no male contribution to the male genome).
 
    The authors of the paper experimented with two species of
wasps, N. vitripennis and N. giraluti. They noticed that when they
crossed individuals from different species, only males were produced.
In other words, fertilization was not occuring. They found out that
this was the result of microorganisms in the cytoplasm of the gametes
destroying the males chromosomes from his sperm. 

    Microorganisms had been seen in the cytoplasm of the eggs of
these species, but this alone did not prove that they were the cause
of the reproductive isolation. So what they did was feed some wasps
food that contained tetracyline, which kills microorganisms, and cross
the wasps again. What they found was, in crosses in which all the
microorganisms had been killed, the two species produced both male
and female offspring. In crosses where the parents gametes still har-
bored the microorganisms, only males were produced in interspecific
crosses. (Note that intraspecific crosses (matings in the same species)
always produced male and female offspring)) Therefore they concluded
that the microorganisms made it unable for the sperm from a _different_
species of wasp to fertilize the females egg. This worked bidirection-
ally (N. vitripennis females to N. giraluti males and N. giraluti fe-
males to N. vitripennis males). The microorganisms did not, however,
inhibit males and females of the _same_ species from producing offspring
of both sexes. 

    The authors then went on to speculate that microorganism
induced reproductive isolation may be a quick way for sympatric
speciation to occur. The paper also list some other cases of sim-
ilar events occuring in other organisms.

REFERENCE:

Breeuwer and Werren, 1990, Microorganisms associated with chromosome
destruction and reproductive isolation between two insect species,
Nature 346: 558 - 560

Subject: evidence for evolution (19 - isopods)
Summary: for female isopods, size doesn't matter
Keywords: isopods, mating success

    In the marine isopod _Paracerceis_ _sculpta_, there are three
discrete male morphologies. These are determined by a single allele
change at one locus. The largest of the three males, the alpha males,
defend harems of isopod females. The intermediate size male, the beta,
mimics female morphology and behaviour and the gamma males, the smallest
of the three morphs, attempt to hide in large harems and not attract
the attention of the alpha male(s). The larger the male, the slower it
matures. But larger males, although they reach reproductive age later
in life, live longer and therefore have more reproductively active
years. In the paper I will summarize here, the authors demonstrate that 
each male morph enjoys equal mating success.

    Male reproductive success in these isopods depends on many
factors. Each male morph is able to sire roughly the same amount
of offspring when isolated from other males. Differences in male
reproductive success occur when males are mixed in the mating 
area, the spongocoel. For example if the spongocoel contains one 
alpha and one beta male, the beta males sires 60 percent of the
offspring. If there is one alpha and a gamma male, the alpha sires
92 percent of the offspring. If there are 2 alpha males and three
gamma males, each gamma males sires 33 1/3 percent of the offspring.
The authors give mating success for 14 different combinations of males 
in the paper (all the combinations they found in nature). 

    They sampled isopods from a natural population for a period
of two years. They found that each male morph had, on average, equal
mating success and the alleles that determined male morphology were
in Hardy-Weinberg equilibrium (HW equilibrium is a measure of how
alleles are distributed in a population.) In the paper they present
a table showing how many spongocoels were sampled with respect to 
each different combination of males. The table also lists how many
females were in each harem. To make a long story short: the numbers
of males, combinations of males and numbers of females added up
such that each male morph was equally reproductively successful.
Below is a summary of some of the data:

male type     mean (+/- se) # of mates number of males

---------       ------------------------         ---------------

alpha         1.51 (+/- 0.08)               452

beta          1.35 (+/- 0.44)               20

gamma         1.37 (+/- 0.23)               83

variance within types = 3.075
varainace among types = 0.003

    Although it appears alpha males have a higher mean # of
mates, the difference is not significant (look at the standard
errors in the beta and gamma males). Notice also that equal
repro success does not mean equal frequency in the population;
it only means that each male type is able to keep replacing itself
in the population. In other words, if conditions stay the same,
the ratio of alpha to beta to gamma males will stay 452:20:83.

REFERENCE:

Shuster and Wade, 1991, Equal mating success among male reproductive
strategies in a marine isopod, Nature 350: 608 - 610

Subject: the "species" red wolf (_Canis_ _rufus_)

    There has been a small amount of discussion about what is a
species here on t.o (and also sci.bio) recently. A recent paper in
Nature presents some interesting food for thought on this topic.

    Wayne and Jenks, in a recent Nature, present a study of
the mtDNA(*) of the endangered red wolf, _Canis_ _rufus_. This
species, once extending over a large range in the southeast, is
now extinct in the wild. The authors examined the mtDNA sequence of red 
wolves (zoo animals and from DNA obtained from museum pelts from 1905 
to 1930) as well as grey wolves and coyotes. (The red wolf occurred only
in regions where grey wolves and coyotes were.)

    When they analysed the red wolf sequences, they found that
the mtDNA was either of grey wolf type or coyote type. This (along
with the geographic information) lead them to conclude that the
"species" red wolf is (was) actually a hybrid of the grey wolf and the
coyote. 

    But wait, the story gets even more interesting. Grey wolves and
coyotes have overlapping ranges in the northern US, but the red
wolf phenotype is not present in hybrids in the north. The red
wolf phenotype is not only a product of the hybridization, but of
environment as well.

    That's just the beginning, however, the red wolf was classified
as an endangered species; but US Fish and Wildlife does not extend
endangered species classification to hybrids. The authors argue,
however, that the "species" former prominence in the food web --
it was the top predator in it's former range -- and the possibility
that the phenotype might not be recoverable by future hybridizations
-- remember, it doesn't work up north -- indicate that the red wolf
deserves to remain classified as an endangered species.

Chris Colby
email: colby@bu-bio.bu.edu

REFERENCE:

Wayne and Jenks, 1991, Mitochondrial DNA analysis implying extensive
hybridization of the endangered red wolf _Canis_ _rufus_,
Nature 351: 565 - 567

(*) mitochondrial DNA -- it's maternally inherited

Subject: evidence for evolution (20 - mutagenesis)
Summary: the poop on directed mutagenesis

    Two new papers examining the phenomena of directed
mutations have recently appeared in the literature. I'll
quickly review these experiments in the next post. This 
post is a short introduction to a few of the classic papers
relevent to this issue.

    In 1943, Luria and Delbruck did an experiment that led
biologists to believe mutations occured at random. They started
many parallel cultures of E. Coli., let them grow, then exposed
them to the bacterial virus lambda. They found that the distri-
bution of resistant cells across all the independent lines was
Poisson. Some cultures had many resistant bacteria, others had
few. If the phage had induced the correct mutation to occur,
each independent line should have roughly the same number of
mutants (a Guassian distribution would be found across all
cultures). (1)

    Lederberg and Lederberg, in 1952, provided another
experiment showing that mutations occured randomly. They grew
bacteria on plates and used round pieces of felt to transfer
bacteria to a replica plate. So, the pattern of colonies growing
on the two plates were identical -- and the corresponding colonies
on each plate all came from a single clone. Lederberg then exposed
one plate to lambda and noted the colonies that survived. Then,
he picked the corresponding colony on the replica plate and grew
it up. All the bacteria he grew were resistant to the phage --
even though they had never been exposed to it. In other words,
the mutation was present before its effect was needed. (2)

    In 1988, Cairns questioned the experimental design of
these studies. He suggested that they did indeed show that
some mutations occured at random, but they did not rule out the
possibility that other mutations could be directed. Lambda kills
bacteria instantly, he reasoned; I'll try the experiment over
with something that will slowly kill the bacteria to see if,
given a chance, bacteria can direct their mutations. His
paper on lactose starved bacteria suggested that some mutations
were directed (i.e. the specific mutation -- and only the specific
mutation -- could be induced by the cell.) However, his study
drew lots of criticism becuase it left a lot of loose ends. (3)

    In 1990, Hall released a data set that expanded on
Cairn's work and met all the earlier criticisms. He showed
that, under stress, some bacteria can induce a mutation to
fix a "broken" gene -- and not produce (many) other mutations.
In other words, the stress was not acting as generalized
mutagen. The needed mutation was occuring far too often to
be explained by random mutagenesis. (4)

    The field is still divided about this topic. I'm
convinced that Hall has demonstrated a class of (seemingly)
non-random mutations. But, in interpreting the possible
impact on evolutionary theory, one must be aware of exactly
what effect has been shown and the distribution of organisms
that can be affected. The only effect shown so far is a
directed mutation rescuing a "dead" gene. Nobody has shown that
directed mutations can create a novel phenotype. 

    In addition, only unicellular organisms (or organisms with 
totipotent cell lines) can have an evolutionary benefit from this 
mode of mutation. Multicellular organisms would need the directed 
mutation to occur in it's germ line cells for it to be evolutionarily
interesting; and germ line cells are the least likely to be exposed to 
the stress. By the time a sperm or egg cell itself is stressed, the 
multicellular organism is probably dead.

    None-the-less, this is a very hot area of research. A
good description of exactly what is happening is being sought,
as well as a mechanism to explain it. Some data indicates that
there are a suite of related phenomena, for directed mutations
have been claimed to: fix single base substitutions, fix frame-
shift mutations and correct large insertion mutations.

Chris Colby
email: colby@bu-bio.bu.edu

REFERENCES:

1.) Luria and Delbruck, 1943, Mutations of Bacteria from
Virus Sensitivity to Virus Resistence, Genetics 28: 491 -
511

2.) Lederberg and Lederberg, 1952, J. Bact. 63: 399 - 406

3.) Cairns, et.al., 1988, The origin of mutants, Nature 335: 142
- 145

4.) Hall, 1990, Spontaneous Point Mutations That Occur More Often 
When Advantageous Than When Neutral, Genetics 126: 5 - 16

Subject: evidence for evolution (20 - Hall)
Summary: summary of Halls PNAS paper

    In a recent paper in PNAS, Hall examined circumstances
where a bacteria needed two independent mutations in order to
survive. He concluded that, in bacteria, mutations occur more
frequently when they are needed than when they are not.

    He experimented on three strains of _E. Coli_ deficient
in the tryptophan (trp) operon. One strain contained a mutation
at position 46 of the trpA gene. The second strain contained
a mutation at position 9578 of the trpB gene and the third con-
tained both mutations. None of the strains could produce trypto-
phan needed for survival or growth.

    He grew up the trpA and trpB strains in media that con-
tained trp so the mutations did not hinder their growth. Then
he spread them on petri dishes that contained all their required
nutrients except trp; so, only cells that mutated could survive
on these petri plates. He examined the plates for evidence of
growth every day for 30 days. As time went on, many revertants
for each strain arose. Hall measured the reversion rate
for both strains (trpA and trpB), and repeated the experiment
using the trpAB strain.

    Now, if the reversion mutations in trpA and trpB
occured randomly, the reversion rate for trpAB should
equal the reversion rate of trpA times the reversion rate
of trpB. Hall found the rate to be 10^8 higher than this.
(Yes, that's significant.

    The revertants Hall found fell into three different
classes (I, II and III). Class III grew the fastest (wild 
type rate), Class II grew slower and class I grew the slowest.
When he sequenced the genes in these revertants, he found that
class III revertants produced the correct mutation such that
the original amino acid was restored to trpA. Class II mutants
produced a mutation such that a similar amino acid was restored to 
trpA -- making it functional enough to save the cell. In class I
mutants, no mutation was evident in trpA -- evidently a suppresor
mutation occured (a mutation in another gene, usually tRNA, to
compensate for another mutation.) In the trpB region, all the
classes had the correct mutation. No other mutations were found
in the regions sequenced. (Hall ruled out the fact that he was
selecting for bacteria with extremely high mutation rates in
another part of the paper -- see the ref if you are interested.)

    So, his data indicates that the bacteria could somehow
induce the mutations they needed for survival -- and only those
mutations. 
I'll summarize a paper by
Cairns that demonstrates adaptive reversion mutations that
involves a frameshift mutation. I'm also preparing a post
about a new example of speciation.

REFERENCE:

Hall, 1991, Adaptive evolution that requires multiple spontaneous
mutations: Mutations involving base substitutions, PNAS 88: 5882-
5886

END
A9-Evolution-Fact-Theory.txt