Demolishing the modern synthesis

Back in July of 1999 I posted a "demolition" of the modern
synthesis. This led to a lively discussion with various
attempts at refuting the demolition and arguments against the
attempt. There was no clear resolution and in the end the
discussion moved to other matters. I thought it would be of
interest to represent the discussion.

This article is organized in several parts. Part I consists of
the original demolition. I have taken the liberty on making a
few minor corrections, and of inserted some marked, indented
paragraphs containing clarifying material. I also have numbered
the paragraphs so as to simplify making references. Part II
contains arguments against the demolition by various persons.
Part III contains counter arguments. Part IV contains an
analysis of the demolition, the arguments, and the counter
arguments. Finally part V contains my comments on the Pimple
Nosed Antarctic Anteater.

Part I: The demolition

(1) There is a fundamental problem with the modern synthesis.
Basically, it is broken. The gist of the matter is that there
aren't enough genes.

(2) The conflict which the synthesis purportedly resolved was a
dispute between the naturalists and the population geneticists as
to the nature of heredity as to whether it was soft or hard,
i.e., whether variation was continuous or discrete. The
compromise was effected by the observation that soft inheritance
(continuous variation) is emulated by hard inheritance (discrete
variation) if a trait is the cumulative
result of a number of genes.

(3) Continuous variation (or emulation thereof) is necessary for
the Darwinian model of natural selection which supposes a process
of accumulating small advantages. It is, moreover, that
which is observed for many traits.

(4) The catch is that there aren't enough genes. The human
genome has approximately 70,000 genes. If genes are to determine
traits quasi-continuously it will take 10-20 genes to control one
trait which means that the number of traits controlled by the
genome is on the order of 5,000 traits OR LESS.

NOTE: The actual number of genes is about 33,000. This
makes the effective number of traits even less. However
the effective number of genes is greater because of various
reading tricks.

(4) The observation that genes affect many traits and vice versa
is not cogent; the issue is one of degrees of freedom. Likewise
appeals to self-organization are not to the point;
self-organization can elaborate the effects of genes but the
variation must be supplied by the genome.

NOTE: This was a point of confusion in the discussion.
Despite the disclaimer, some assumed that I was arguing for
a direct gene to trait mapping. I was not. However the
model used in the modern synthesis does implicitly assume
presume such a mapping.

(5) It is relevant to point out that a gene on average consists
of a thousand base pairs, thereby supplying many bits of
information. However most of this supply of information is a
mirage. The vast bulk of a protein is devoted to folding up into
the right shape. The region of interest is the hot spot which
only consists of a handful of amino acids. It should also be
noted that a fair percentage of the genome is devoted to
house-keeping machinery for the eukaryote cell.


NOTE: This is oversimplified in that changes in the base
pairs that dictate the folding are relevant. None-the-less
the effective number of bits in a gene is far less than
the nominal number.

(6) The problem then is that a few thousand (or less) evolvable
traits is not enough to account for the evolution of the
morphology of human beings and our fellow vertebrates. It does
seem to be true that the synthesis accounts for the evolution of
bacteria (and presumably the monera) - the number of traits to be
governed is much smaller and the effects of the genome are
strictly localized. However the synthesis was developed to
account for the evolution of the metazoa and the metaphyta in
terms of population genetics and this, manifestly, is what it
does not do.

Part II - Arguments against the demolition

Several people argued against the demolition, the principal
arguments being those of PZ Myers and Wade Hines.

The arguments of PZ Myers:

1. The combinatorial argument. N genes don't code for just N
traits, they can code for 2^N traits. That is, one gene allows
for 2 possible cell states, 2 allow for 4 states, 3 allow for 8,
etc.

2. The regulatory argument. What's critical in defining a cell
is its regulatory state -- and any one gene may have a large
number of regulatory sites. (OK, it's a variant of #1...)

3. The development argument. Genes aren't adequate to specify
an organism-- there are also significant influences from the
cytoplasm and the environment, and each cell has an independent
history that influences gene expression.

What it amounts to is that your argument was a rather more subtle
and cleverer- than-usual variation of the creationist demand that
we show "fin genes" that get turned into "arm genes". You were
making an unrealistic assumption that there is some kind of
simple one-to-one mapping of genes to discrete morphological
traits, and there isn't one. There is no "arm gene". Similarly,
for Bubba, there is no "7,351st Purkinje cell from the midline on
the left side of the cerebellum gene".

Wade Hines argued against the need for continuity of genetic
determination as follows:

There isn't a need for continuity of genetic determination.
The key is of course additive advantages and not continous variation.
More to the point is that potential advantages need to be available
for selection. That is rather broad and deep with a suspect smell.
A lack of determinancy of phenotype from genotype slows selection
and at some point leaves drift as the dominant factor. But I don't
see that continuity is required.

Hines continued with an example:

Let's try to start on a real example. What's involved in the
"fight or flight" response. We get (partial list) a release of
adrenaline, binding of adrenaline to a receptor, G-protein
activation, G-protein inactivation, scavanging of adrenaline and
various cascades of 2ndary messages.

Focusing on the receptor which bind adrenaline, there may indeed
be only a handfull of amino acids which form the actual binding
pocket but the whole rest of the molecule can participate to
provide nearly continous variation to binding affinities.

The G-protein which is activated only has a few amino acids
which participate in the converison of ATP to cyclic ATP but
the rate of that conversion is subltly affected by the
rest of the protein. Elsewhere that protein has a delayed fuse
that will hydrolyze a GTP to a GDP and then turn off the
production of cAMP. That clock can also be tweaked by subtle
effects elsewhere which can be independent or interdependent
to the rate of cAMP formation. Likewise we have multiple
routes to varition in the scavanging of Adrenaline or its
release concentration, the concentration of the receptors
themselves, their ability to reprime for the next response
and on and on.

All of these and more contribute to the difference between
acting like a sloth which slowly turns around to see who
just ate its hindquarters and a shrew that runs and hide
from the sound of a butterfly landing on a bush 10 feet
away.

Part III - Counter arguments to the objections

Myers's arguments (1) and (2) were non-starters based on a
misunderstanding of the concept of degrees of freedom. There was
a bit of discussion back and forth, but the following explanation
seemed to work as a clarification.

...It is given that there is a messy map from the genotype to the
phenotype (and even that the phenotype is a function of the
environment as well.) The key is the number of degrees of
freedom, i.e., the dimensionality of the two spaces. If there
are N dimensions in gene space they can determine at most N
dimensions in trait space. This is not changed by the messiness
of the mapping....

We are not, repeat not, repeat NOT, talking about a one-to- one
mapping of genes to traits. We are talking about the number of
variables (on the gene side) and the number of function values
(on the trait side). The variables are independent of each
other. The function values are not, in general, independent of
each other. To give a simple example:

Suppose we have two variables, x and y, and three functions f, g,
and h which are given by:

f = x+y
g = x - 2*y
h = 2*x - y

We have three functions and only two variables; the
dimensionality of the function space is apparently three (three
different functions) but in actuality is only two because the
three functions are not independent. That is, we can express h
as a combination of f and g. The situation is general. If we
have N independent variables and M functions of them (M>N) we can
have at most N independent functions; the remaining M-N ones can
be expressed as combinations of N of them.

I argued against Myers's "information in the cytoplasm" argument
at the start of his third point as follows:

This also doesn't work although the issues are subtler. The
problem is that development is not heritable. Consider a parent
organism creating an egg. The parent not only passes on a
genotype, it also passes on an environment in which the child
organism will develop. Fine, this apparently is information that
is not in the child's genotype. Consider, however, what happens
when the child in turn creates an egg. It must supply the same
developmental environment to its offspring. Now where does that
information come from? There are two possibilities. One, which
is actually the case, is that the information is encoded in the
genome. (I.e., a mother inherits genes from her mother that
"describe" how to create the eggs environment. There is some
interesting genetics there.) The other, which is not the case, is
that it has recorded somehow the information about the
environment given it and sets up the same environment for its
offspring. The latter possibility, if it were to occur, would be
a form of direct Lamarckian inheritance.

Information in the cytoplasm which is under genetic control, even
indirectly, counts as information in the genome - you need genes
for it. If you are going to talk about *additional* information
in the cytoplasm you are talking about *nongenetic* information.

I argued against Hines's "no need for genetic continuity"
argument as follows:

Continuity or a reasonable approximation thereof is required.
("Was" - we are talking about the synthesis as formulated.) It
was and is the biologists, the ones that actually study plants
and animals, that demanded soft inheritance because that is WHAT
IS OBSERVED. Yes, there are traits that exhibit hard inheritance
- color of eyes, for example, and smooth vs wrinkled peas. There
are a lot of traits that are effectively continuous (I presume
that we all understand continuity can be approximated by additive
combination). We need only mention some examples, e.g., height,
the size of a finch's beak, and the placement of jawbones in
therapsids.

And made the following remarks about his example:

Now this actually is a good argument, the essence being that
variations in the protein structure supply de facto continuous
variation in function. There are problems, though.

For this to work (in the context of the synthesis) it is
necessary that there be sequential incremental change. Thus
suppose we have a molecule X which controls a rate. There will
be accessible (by mutation) variants X.1, X.2, etc. all of
which, for Darwinian selection to work effect small changes in
rate. Of these some one (or few) are selected, say X.1. In turn
new variants arise, X.1.1, X.1.2, etc. The same requirement
holds here. Thus the approximation of continuity must hold not
only at the base point X but also in the space that X is resident
in. This is a strong requirement.

Part IV - After thoughts

I think the upshot is that the demolition is correct, sort of.
PZ Myers put it this way:

Does this spell trouble for the "change in allele frequencies"
mantra? Sort of, I think. Ultimately, it's all going to come
down to some messy molecular biology, but for now there is more
complicated stuff going on than we can understand. Look at beak
size in those finches, for instance -- it's variation that can be
quantified with a few simple parameters, but all the underlying
biology is a total mystery. How is shape and size of a beak
specified? I doubt that there is a "beak gene" anywhere in the
bird. There are genes that somehow specify growth rates in
certain bones, genes that define adhesivity in migrating tissues,
genes that allocate cells to certain fates. You can measure beak
length, but there are a thousand sneaky changes beneath that that
you don't see at all -- and who knows which one is the genuinely
significant one that selection sees.

What it comes down to is that the model of genetics that was
worked out in the first half of the twentieth century is wrong.
The confusing thing is that it works, at least until you get down
to the nitty gritty of the underlying biology. What has
happened, so to speak, is that life evolved mechanisms to make it
possible for Darwinian evolution to work.

The demolition and the discussion raised the issue of
information: How much heritable information is there and where
is it. Myers made a point that there is heritable information in
the cytoplasm, i.e., information that the mother passes directly
to the egg that is not in the genome. Gene imprinting is an
example; development directed by maternal hormones is another,
e.g., the testerone shot that mothers give their male fetuses.

I made the counterpoint that for this information to be stable it
must ultimately be derived from information in the genome.
Information that is part of the cell's dynamic processes degrades
over a few generations at most.

It occurs to me that this is a good thing, that much of evolution
(or at least what looks like evolution) has very little to do
with changing alleles. Consider those finch beaks again. To
make it simple lets suppose the mother adds a hormone to the egg
that controls how big the beak will become - and that she puts in
about the same amount that her mother put in her egg.

The effect is that there will be a lot of variation in beak sizes
without any underlying genetic variation. Darwinian evolution
can operate very quickly on that variation, much more quickly
than it could on genetic variation.

What this means is that there can be mechanisms for quickly
changing phenotype attributes within a few generations to respond
to environmental changes.

It also occurs to me that there may be rather less information in
the genome than one would suspect from observing the phenotype.
After all, most animals are simply variations of the segmented
tube with things sticking out.


Part V - The Pimple Nosed Antarctic Anteater


There is a bit of confusion here. Let's suppose frex that the
Pimple Nosed Antarctic Anteater has a colored pimple on its nose
which is controlled by three genes which we shall very originally
call alpha, bravo, and charlie. Furthermore alpha has two
alleles a and A, bravo has two alleles b and B, and charlie has
two alleles c and C. The color of the pimple may be any one of
eight hues; i.e., the pimple color is the trait and the hue is
the value. So what we have is an exponential growth in the
number of possible values that a trait might assume. So far, so
good.

There is a catch. For population genetics to give us anything
besides drift we need non-zero selection coefficients for genes.
To do this what we really need is that similar phenotypes (at
least as far as fitiness is concerned) have similar genotypes.
Thus, suppose that purple pimple noses are particularly favorable
and that genomes Abc, aBc, and abC all produce purple pimple
noses. Unfortunately genomes ABc and AbC produce green pimple
noses which are the favorite diet of the Antarctic Fly Trap and
Antarctic Anteaters with aBC genome are, ahem, obligate
homosexuals. There is a further complication. In some years the
Antarctic Grasshopper swarms; it dines exclusively on purple
pimple nosed Antarctic Anteaters and on the Antarctic Fly Trap.
In those years green is in and purple is out. We have this
problem that colors do not generally breed true.

The situation is worse with respect to the synthesis and soft
inheritance. In traits with soft inheritance (if there were such
a thing) the trait has a numerical measure(s), e.g., the size of
the bazoonga. [This being a family group we shall not discuss
what a bazoonga is or what it used for.] The offspring have
bazoongas whose size varies around the mean of the size of their
parent's bazoongas. Finch beak size will do as an example. The
point is that natural selection in the Darwinian formulation
operates on traits with soft inheritance. The explanatory
stories - the exaptations, the evolution of the angler fish's
bait - all rely on the accumulation of small favorable
variations. These in turn depend upon the determination of
traits being approximately additive.

If genes in general encoded trait values and there were no
correlation between fitness values and alleles, i.e., to get a
fit genotype you have to have the whole sequence exact, selection
of genotypes would quickly break down because there would be too
many different genotypes.

Richard Harter, cri@xxxxxxxx
http://home.tiac.net/~cri, http://www.varinoma.com
Save the Earth now!!
It's the only planet with chocolate.

.

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