Re: Ernst Mayr: Where Are We (1976)
- From: "John Edser" <edser@xxxxxxxxxx>
- Date: Fri, 3 Jun 2005 13:39:02 -0400 (EDT)
"Perplexed in Peoria" jimmenegay@xxxxxxxxxxxxx
> > JE:-
> > Given the empirically true fact that all genomic gene fitness in
nature
> > remain epistatic and therefore 100% dependently selectable whereas
the
> > opposite is assumed within population genetics oversimplified models
> > that have ended up providing evolutionary theory with everything
from
> > Haldane's (false) Dilemma to Hamilton's heuristic rule that was
misused
> > to determine when organism fitness altruism could evolve in nature,
> > where are we now in 2005? Why hasn't a theory of heritable epistatic
> > gene fitness been developed allowing a minimally VALID simplified
model
> > of TWO loci with two alleles that are dependently and not
independently
> > selected at the empirically true, single, fertile organism level of
> > selection?
> JM:-
> Because it is an "empirically true fact" that epistatic gene fitnesses
> (as you seem to use this term) are not heritable.
JE:-
Mayr is discussing the same point that I have been making for more than
5 years. Polygenetic traits empirically exist (traits whereby the
phenotypic is simply the addition of each gene's effect + or - e.g.
human height) allowing each gene to have an independent effect. However
the FITNESS of the trait is NEVER the simple addition of the fitness of
each polygene disallowing any assumption that the FITNESS of each gene
is independent. It remains incorrect to infer that because polygenes
exist polygenetic fitnesses also exist. Not one single additive in gene
fitness trait has ever been documented in nature yet population genetics
models assume that the fitness of one gene can simply be added to
another.
> JM:-
> There do exist models of two epistatic loci dependently selected at
the
> organism level.
JE:-
The "organism level" is not empirically sufficient but the fertile
organism level is where these levels are not at all the same.
Epistemologically: all models remain simplifications/over
simplifications of an existing valid theory. Gene centric Neo Darwinists
always refuse to just name the theory these models were simplified/over
simplified from i.e. their models are attempting to replace valid
theory. Model results have to be corrected by the theory they were
simplified/over simplified from in order just to make any sense. So far
they remain uncorrected because a multilevel theory has never been
proposed. More than just the mere suggestion that multilevels of
selection exist is required to produce a valid theory of same. To my
knowledge nobody has even attempted to provide a minimal dualistic
theory, i.e. how two independent levels of selection could possibly
operate in nature. All sorts of problems have been ignored.
Are these two model independent levels selected simultaneously or
serially? If simultaneously how is such an event even possible? If
serially what happens when they compete? Does the first level to be
selected dominate the other? What is the missing multilevel theory Neo
Darwinistic models were simplified/over simplified from and where are
the required missing theory corrections for all these model multilevel
results?
> JM:-
> The key issue in such models is the degree of linkage
> (segregation independence) between the two loci. It turns out that if
> the loci are unlinked (on different chromosomes, say), then
> **under the assumption of random mating**
> the process of recombination undoes any linkage disequilibrium created
> by selection.
JE:-
Linkage and fecundity rates (the rate of reproduction of sterile
immatures) determine the probability that two alleles at two different
loci may be inherited together within just a sterile immature body. When
a female tick, which can only reproduce itself once, mass produces about
10,000 sterile immatures and then dies, many recombination events are
represented in these immatures. What matters is which of these 10,000
are raised to fertile adulthood and _exactly_ how is each gene is
actually selected in nature. In this species only about 2.something
sterile immatures are mostly raised to fertile adulthood, i.e. just a
tiny fraction of the fecundity rate. The mass of infertiles that die
along with their gene combinations are only subject to a process of sub
selection and not selection because they are only dependently and not
independently selectable. This means that high fecundity rates can be
advantageous because they allow the less costly act of sub selection of
the better epistatic gene combinations. Sub selection is more efficient
than selection because a selection of them would require immatures to be
raised to fertile adulthood so they acquire an independent fitness.
> JM:-
> Hence, the standard "independent selection of loci" model
> are close to correct, as long as you allow the fitness of alleles at
one
> locus to depend upon the frequency of alleles at another locus.
JE:-
These models do not distinguish between fertile and infertile forms so
they have no way of discriminating between the much more costly act of
independent selection from the much less costly act of the dependent sub
selection of expendable sterile immatures.
> JM:-
> On the other hand, if the loci are tightly linked (close together on
the
> same chromosome, say), then recombination will disrupt the linkage
> disequilibrium only rarely. Under these circumstances, you can think
of
> the two loci (each with two alleles) as a single locus (with four
alleles)
> and the situation is again well handled by the standard models.
JE:-
Since the overwhelming majority of genomic loci are empirically
homozygous 2 epistatic genes within most two locus two allele dependent
fitness models can be inherited together. However, only the heterozygous
exception is discussed. Apparently the much more common homozygous event
is regarded as less interesting yet it is more compelling for the
heritability of epistatic gene fitnesses.
> JM:-
> Models exist for the cases of close (but not too close) linkage, but
they
> are not exactly *simple* models. Models also exist which relax the
> assumption
> of random mating, and which thereby make the epistasis somewhat
> "heritable"
> in that way. These models are definitely NOT simple.
JE:-
All empirical gene fitnesses remain epistatic no matter what model
attempts to dictate that they "cannot be". Any model that deletes such a
basic empirical fact has to be defined as "oversimplified"_. The non
correction of oversimplified model results via the theory it was
oversimplified from constitutes a gross misuse of that model. My example
remains Hamilton's Rule. Here relatedness r^e has to set e to be
minimally 2 and not just 1 because all empirical gene fitnesses are
epistatic requiring a minimum of two dependent loci. The variable e must
be minimally set to 2 if the rule is not to be just a non representative
oversimplification. Unfortunately, in this case the rule fails (even as
just a 100% relative proposition).
My epistemological objection has always been the same. I am happy to
accept simplified/over simplified models as extremely useful tools to
help understand/test the scientifically valid theory they were
simplified/over simplified from, but only after any model result has
been corrected by the parent theory. Quite obviously, models cannot
contest or replace their parent theories. Yet, this is exacty what has
happened over the last 50 years as mathematicians replace biologists
within evolutionary theory so that Popper becomes discarded as
irrelevant to just the mathematics.
> JM:-
> As I understand it,
> this is the kind of issue which distinguishes Wright's view of
selection
> in structured populations from Fisher's view of selection in
well-mixed
> populations. One of these days, I am going to have to dig up a good
> tutorial on Wright's F-statistics and see how they work.
JE:-
I think the main difference was that Wright allowed drift to produce
many isolated sub populations that allowed the testing of drifted
epistatic gene combinations within each sub population before they
remixed with the main population.
> JM:-
> You also demand that the models work at the "fertile organism level of
> selection" rather than just at the "organism level". I understand
this
> to mean that the selective fate of an immature organism is taken to be
> a function of its parents' genomes, rather than its own.
JE:-
I do not "demand it", empirical science does. Fitness remains the only
common point of test of any evolutionary theory so far proposed that can
be tested. The focus of gene centric Neo Darwinism is entirely
individual gene fitnesses. Genomic genes are not selectable within
immature sterile forms for the obvious reason that these forms have no
heritable fitness until they become fertile. However the same genes
remain selectable from whence they came: within the fertile bodies of
the parents that provided them. It remains biologically incorrect to
regard sterile immatures as equals to fertile forms simply because gene
centric models require them to be so. Immatures are entirely at the
disposal of their parents because the genes in their bodies can only be
dependently selected via their parents Total Darwinian Fitness (TDF).
Eusocials are not unique. They prove that selection on just fertile
forms can enslave immatures for the TDF benefit of their parents (and
the sterile forms because they remain TDF dependent) but only under
enclosed nest conditions where a controlling pheromone can circulate.
> JM:-
> But this is also
> empirically untrue, at least in part. While the parents' genomes are
> important (in plants and in animals with parental care, at least), the
> genome of the immature organism is different from that of its parents
> and it is very important in determining the fate of the immature
organism.
JE:-
Yes, but their fitness fate remains _entirely_ with their parents TDF
until they become fertile themselves. The genes within infertile forms
remain entirely non heritable until that form actually becomes fertile.
Only at this one, exact point can the epistatic fitness of their gene
combination even possibly become subject to natural selection. This
basic remains deleted within most models that simply assume independent
gene fitnesses where the results of such a model oversimplification
remains uncorrected, e.g. Hamilton's rule where e remains fixed to 1 and
not minimally 2 within relatedness r^e.
> JM:-
> Models which make selection dependent upon two or three genomes are
> definitely NOT simple. They are also unnecessary, since Hamilton has
> shown us how to work with a simple model in which the *inclusive*
fitness
> of an organism is taken to be dependent upon only its own genome.
> I invite people who understand pop gen better than I do to comment
upon
> my summary.
JE:-
Understanding how gene fitness epistasis can be coded and inherited
remains one of the biggest challenges of biology. It does not help to
just delete this problem within uncorrected oversimplified models and
then declare the problem solved. Hamilton's model deleted all epistasis
yet empirical gene fitnesses remain epistatic no matter if Fisher
dictated that they can't be. Any valid theory must fit the facts and not
the reverse. In reality each competing allele within Hamilton's model
actually represents one entire fertile form. For his model to even
approach biological reality e within r^e must be minimally set to 2 and
not just 1. Assuming e=1 allowed e to be invalidly deleted and then
forgotten.
Haldane's Dilemma was proven false. No dilemma empirically existed. Yet,
nobody even thinks of correcting the oversimplified modelling
assumptions that provided Haldane's false dilemma. Why?
Regards,
John Edser
Independent Researcher
PO Box 266
Church Pt
NSW 2105
Australia
edser@xxxxxxxxxx
.
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