Re: Hamilton's rule
- From: "John Edser" <edser@xxxxxxxxxx>
- Date: Thu, 1 Dec 2005 00:21:18 -0500 (EST)
Bob O'Hara wrote:-
> > JE:-
> > The deletion of all gene
> > fitness epistasis within population genetics because the Hardy-Weinberg
> (HW)
> > bi-nominal expansion required it has never been corrected.
> You could just as well write "The deletionof all fitness within
> population genetics...". You would then be arguing that we have deleted
> all fitness from population genetics, an argument that is just as valid.
JE:-
Total Darwinian Fitness (TDF) has been deleted from all of population
genetics yet TDF remains the only way that evolution by natural selection
within a natural population can be halted experimentally, i.e. TDF is the
only _empirically_ based measure of fitness that actually exists within the
_science_ of evolutionary theory simply because it offers a possibility of
definitive refutation and not just a non definitive non verification and can
halt non random Darwinian evolution by natural selection leaving only random
processes like drift and mutation.
Epistasis can refer to two quite separate concepts within _empirically_
based evolutionary theory:
1) Epistasis with regard to the expression of one trait. This is the well
understood fact that more than one gene is almost always required to code
for one trait. The only exception is one polypeptide defined to be one
trait. Almost without exception, biological traits are composed of more than
just the one polypeptide so almost without exception, all genes are coded
for in an epistatic way.
2) Epistasis with regard to the FITNESS of any one expressed trait, i.e. not
just trait formation. This is the little understood fact that every genomic
gene remains entirely fitness dependent to every other gene within the one,
same genome. Even though traits may be coded by genes in a simple additive
way allowing each genes effect to remain constant and therefore independent,
e.g. polygenetic traits such as human height, at no time is the fitness of
any one of these polygenetic genes also additive and therefore constant and
independent. Not one single case exists within nature wherein the fitness of
one trait is just the simple addition of the fitnesses of each gene that
codes for it.
> You're also up agoinst history: the first paper on natural selection in
> Mendelain populations (Fisher, 1918) included epistasis.
JE:-
Firstly, epistatic trait formation was not differentiated from the epistatic
FITNESS (1 and 2 above). Secondly, additive effects between genes which
represents zero epistasis because any additive effects remain constant and
therefore independent became "additive epistasis" which is just a
contradiction in terms:
http://www.nature.com/hdy/journal/v95/n6/full/6800699a.html
Here is a quote from the above website provided by Jim Menegay which
provided access to the paper:-
Quantitative trait loci: Mapping the future of QTL's by D Erickson,
Laboratories of Analytical Biology, Smithsonian Institution, Washington, DC,
USA
"Efforts to analyze quantitative traits have focused on answering sets of
related questions in two general areas. The first is 'the distribution of
gene effects', which addresses the number of genes affecting a trait, their
relative contribution, and physical location within the genome. The second
is 'the mode of gene action', which focuses on establishing if a gene's
effect on phenotype is constant (an additive effect), or contingent upon
interaction with other genes (epistasis), the environment (GxE) or
participation in multiple phenotypes (pleiotropy). Thus, we can categorize
gene effect as additive vs nonadditive.
These nonadditive gene effects are the hobgoblins of quantitative genetics,
since they greatly complicate any attempt to dissect the genetic structure
of complex traits. Yet they also have tremendous evolutionary implications,
with the magnitude and prevalence of epistasis being one of the basic
unanswered questions in evolutionary biology.
Thus, we can outline two extremes of genetic architecture (distribution of
effects+mode of gene action) that determine a quantitative trait. In the
first, a moderate number of genes each have a relatively large effect and
all are strictly additive. In the second, a large number of genes
contribute, each with a very small effect on phenotype, and each exhibits
varying degrees of nonadditive interactions. The former would expedite our
decomposition of quantitative traits into their component loci; the latter
would complicate it.
These new data from Kroymann and Mitchell-Olds certainly suggest that the
more complicated genetic architecture underlies quantitative traits. Indeed
the authors' identification of this locus was entirely serendipitous, and
the two loci would not be detectable in typical genome scan of loci
affecting growth rate. This suggests that were one to carefully analyze many
other such small intervals throughout the genome, then one would find many
such small effect loci exhibiting complex nonadditive behavior contributing
to the genetic basis of the trait we seek to describe."
JE:-
Hamilton's Rule (the subject of this thread) deletes ALL epistasis including
all fitness epistasis for his single organism-fitness-altruistic-allele
including all gene fitness epistasis because Fisher et al deleted all
epistasis (all non additive effects) by defining that only additive effects
between genes are actually heritable. I have re-included gene *FITNESS*
epistasis within HR as r^e where e is minimally equal to the number of
chromosomes in the species inclusively selecting. The simple fact remains
that the empirical FITNESS of Hamilton's single allele remains dependent on
and not independent of, at least one gene on each chromosome where the
probability r on inheriting each one of them using normal sex has to be
multiplied.
Waddington included the new variable "developed in x" within Haldane's basic
population genetics equations (which were based on the Hardy-Weinberg
bi-nominal expansion of just two alleles at one locus) over 50 years ago
allowing at least some representation of non additive epistatic effects
within population genetics. Why don't you review Waddington's
ignored-for-about-50-years-hypothesis here with special regard to
Waddington's pioneering effort in including at least a modicum of real
epistasis within HW (Felsenstein can provide you with the reference)?
Regards,
John Edser
Independent Researcher
edser@xxxxxxxxxx
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