The hole in the bucket.
From: John Edser (edser_at_tpg.com.au)
Date: 01/24/05
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Date: Mon, 24 Jan 2005 11:55:45 -0500 (EST)
Joe Felsenstein wrote:-
> >> . . . my children have half copies of my genome
> >> (r = 0.5) so a certain amount of parental care
> >> looks like it would be in my interests. But my
> >> nephews also have partial copies of my genome
> >> (r = 0.25) so, . . .
> >Did anybody else notice that Perplexed fell back
> >into Haldane's fallacy? It's subtle, I know, but
> >that's why it's so difficult to overcome.
> >Perplexed, both your children and your nephews
> >have copies of over 99.9% of your genome.
> JF:-
> There is no fallacy but some slightly misleading terminology.
> When someone says that my genome is 50% similar to my
> brother's they are thinking not of DNA-level similarity
> (which is 99.9%) but of Identity by Descent. This isn't
> always made clear.
JE:-
The _biological_ parentage of any IBD related gene
is not defined. This is not just "slightly misleading"
is hopelessly ambiguous. Is the IBD parent one gene
or one organism? Perhaps you argue that it makes
no difference because you have deleted all gene
fitness epistasis. If you do, then you are correct,
if and only if, you only refer to a simplified model
and not the _empirical_ theory from which the heuristic
model was derived by simplification. This is because
not one single linear (independent) gene fitness
has ever been documented within nature. NOT ONE!
Such a fitness is required if relatedness IBD (which
is actually r^e) is to be simplified to just r^1
because e has to remain fixed at e=1 within
the model to allow gene fitness independence.
In nature it is _always_ > 1 disallowing
any gene fitness independence. So what do we
observe in nature: just NON linear (dependent)
i.e. epistatic gene fitnesses. How unexpected!
> JF:-
> For a rare allele in a population, if I have a copy of it
> (i.e., conditional on my having a copy) the probability
> that my brother has a copy of that allele is 50%. If we
> look at the sequences of the two different alleles, they
> might be similar in all but one of their nucleotides. But
> the probability that my brother carries the same exact
> allele (i.e. identical in all of its bases) is 50%.
JE:-
So what _parentage_ are you inferring from this probability?
If one gene is the rightful parent, one organism or neither?
Does it matter? If you say nothing, which I am
sure will, you allow an ambiguous
selectee situation to arise whereby you can skip
from parent organism to parent gene and then back again
with impunity to evade any test of your proposition.
A neat, but very old trick. Ladies and gentlemen
which one of 3 shuffled cups will uncover the green
pea of IBD relatedness, the organism parent cup,
the gene parent cup or the cup: none of these?
Now watch carefully ... nothing up my sleeve....
> JF:-
> A connection between these two notions is provided by
> looking at the number, not of similarities, but of
> differences. I differ at 0.1% of my nucleotides from
> a random other individual. But I differ only 0.075%
> from my brother. That is 25% less, so less by a
> fraction equal to half of the Identity by Descent.
> (The half is because when we look at a random copy at
> a particular locus in me, and one in my brother, one
> might come from our father and the other from
> our mother).
JE:-
Is the parentage of selfish genes
not now allocated to EVERY
GENE, just a tiny 0.1% fraction of genes that
are different between random individuals
of the same species in one population?
Does this 0.075% from a brother
which is "25% less, so less by
a fraction equal to half of the Identity
by Descent" allow r within rb to be
IBD or NON IBD, or a mixture of BOTH?
> JF:-
> Incidentally, Haldane did *not* say that he was 50%
> similar to his brother. He is supposed to have said,
> in response to the question of whether he would lay
> down his life for his brother, "No, but I would for
> two brothers or eight first cousins". (Which was theoretical
> because he had no brother, but did have a sister, the
> novelist Naomi Mitchison).
JE:-
Yes Haldane employed genes IBD and not genes
related NON IBD simply because genes NON IBD
cannot work because relatedness, vebe between
sepecies becomes much too high.
However like all the
others after him Haldane never ever specified if
the gene is now the designated selected parent,
the individual, both or just neither.
Haldane just infers, like Hamilton
et al, that a heuristic independent
gene fitness can force organism altruism at
an _empirical_ Darwinian fertile form level
without ever stating what Haldane's total
Darwinian fitness was supposed
to be and in what units it was to be
measured in.
If Haldane scarifies himself for
"two brothers or eight first cousins"
where can these _amazing_ selective events reside?
The genome level, the fertile organism level, both
or neither? If Haldane could have had say 3 normal
children all maximally related 0.5 to himself
without the massive wastage of proxy reproducing
random individuals (see Prof. Felsenstein's example
where he calculated a 50% cost for this wastage
within a worked example) but he is killed
helping just two, why would nature ignore the
one extra fertile form he could have normally
reproduced if his fitness mathematics had not
been so utterly incomplete and parental
ambiguous?
Why doesn't Felsenstein point out that
attempting to correct the massive wastage
of reproduction by proxy (which is _not_ paid
using normal reproduction) via genome matching
for Hamilton's selfish gene, e.g. Dawkins
popular Green Beard model, entirely fails because
of an inflationary (geometric) epistatic cost
that suddenly becomes evident:
(r^e)b
Hamilton only _artificially_ pegged to e=1 within
Hamilton's Rule in order to engineer for
himself a heuristic independent genome level
of selection.
Is Felsenstein happy about the fact that most of
his incompetent colleagues commonly confuse Hamilton's
Rule with Haldane's Pub Rule which preceded it? Is he
aware that b within Haldane's Pub rule is the
number of recipients helped but within Hamilton's
Rule b is the number of offspring of a unspecified
number of recipients helped where this must be one more
generation removed? This confusion only allows
a 0.25 relatedness to proxy recipients to be a maximum
and not 0.5 IBD? This make s a _massive_ difference
for maximal kin selective events doesn't it....
Felsenstein has stated he can derive Hamilton's
Rule from classical group selection. Would he
tell sbe reader's what this means to evolutionary
THEORY after Hamilton's Rule was wheeled out
over 50 years ago to replace classical group
selection because it had failed? No? Ok, I will
inform them. It means Hamilton's Rule was
always just another version of classical
group selection which contained a fatal error.
Group relative fitness was only measured by comparing
group sizes and not the total number of fertile groups
reproduced from each group as the parent within one
population of same. Surely a person of Felsenstein's
stature understands that differential group sizes
can only reflect contesting differential total
Darwinian fitnesses WITHIN each population, i.e.
no group selection was ever involved just ordinary
Darwinian selection? This means Felsenstein
has derived Hamilton's Rule
from (surprise surprise) Darwinian theory!
What then is the refutable maximand fitness that
exists within Darwinian theory? Total Darwinian
fitness, of course. So, what did Hamilton et al
deliberately delete to create their heuristic
fitness world? Surprise surprise, total Darwinian
fitness. What cost alone allows the sign of
c to become non arbitrary when an ongoing rb fitness
becomes forced to conclude within Hamilton's Rule?
ONLY the deleted cost c(max). And, what is this equal
to? Surprise surprise, total Darwinian fitness!
What is the only fitness measure that can refute
evolutionary theory? Surely not again, yes, it's
Darwinian total fitness. What is the only fitness
that Felsenstein et al flatly refuse to discuss?
You guessed it: total Darwinian fitness.
What is the only possible way that total Darwinian
fitness could be inherited? Via non linear 100% epistatic
gene fitnesses, which were all deleted by Fisher.
Which model was Hamilton's headless model, descended
from? Fishers. And who was Fisher attempting to make sense
of? Darwin.
There's a hole in the bucket dear Henry dear Henry....
My Regards,
John Edser
Independent Researcher
PO Box 266
Church Pt
NSW 2015
Australia
edser@tpg.com.au
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