Re: Washburn's fallacy
From: Perplexed in Peoria (jimmenegay_at_sbcglobal.net)
Date: 01/17/05
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Date: Mon, 17 Jan 2005 00:53:32 -0500 (EST)
"John Edser" <edser@tpg.com.au> wrote in message news:csbo4u$2c3a$1@darwin.ediacara.org...
> JE:-
> Genes IBD measures the probability that
> one gene AS A SELECTED PARENT, i.e. as
> an independent REPRODUCER of genes, may be
> the parent of another gene within another
> body.
I think you meant to say "the *ancestor* of another
gene in another body.
And, it is more complicated than that, as I think you
realize. Consider the IBD relatedness between me
and a full cousin. We share two recent common
ancestors - two grand parents. The probability that
I inherited a particular gene from our grandfather is
1/4. The probability that my cousin inherited the same
gene is also 1/4. The probability that BOTH of us
inherited that gene is 1/4 x 1/4 or 1/16. But so far
we have only dealt with our shared grandfather. Our
shared grandmother contributes another 1/16 to the
IBD total so that my relatedness IBD to my cousin is
1/16 + 1/16 = 1/8. I need to save 8 cousins from
drowning to get a free lunch at Haldane's pub.
> Thus two and not just one criteria
> apply to relatedness IBD:-
>
> 1) The genes must be the same genes.
> 2) They must share a lineage.
Where lineage must be defined as a trip up the tree
followed by a trip down. (Up from me to our grandfather,
then back down to my cousin.) My cousin and I share two
lineages, but if we share (IBD) only one copy of the gene
for altruism, then it can only have come from one of
those two lineages. But it could have come from either -
that is why we had to add the probabilities.
> Clearly, two genes may be the same gene but
> can be very closely or just distantly related.
> If the gene is closely related in a normally
> sexual species then the maximum probability
> that it is the very next in the lineage to
> a defined gene parent is 0.5. Here relatedness
> only means how close along the lineage
> one gene can be said to be to another.
> Washburn gets 1) but not 2) which remains the
> more critical because IBD now defines each gene
> as an _independent_ unit of selection.
> This means that all genomic genes IBD
> must compete at a supposed independent
> level of selection AGAINST every other gene
> within the same genome allowing fitness altruism
> to be selected for at a higher level of fitness.
Hmmm. I would have said that a gene lineage competes
against every other lineage at the same locus. Not
against every other gene in the genome. After all,
there is no way that it can WIN against genes at
other loci.
Could you explain the reasoning why you say that
it is competing against genes at other loci?
If we were discussing meiotic drive, I could maybe
see it, but we are not; we are discussing altruism.
> In Darwinism genes do the exact opposite.
> They can only cooperate to provide a fitness
> gain at ONE higher level: the fertile organism
> level. The most important role that relatedness
> IBD plays is it's implicit identification of the
> gene as THE selectable parent because
> genetic epistasis has been entirely
> deleted within Hamilton's
> IBD calculations. If you include
> just a little of it each genes IBD
> relatedness has to be _multiplied_.
> The probability that two alleles at
> two different loci have reproduced two
> others within one other body is maximally
> 0.5^e where e=2 reducing r to just 0.25. The
> more alleles at different loci that you allow
> to calculate an IBD epistatic relatedness
> reduces the maximal possible IBD relatedness
> and therefore Hamilton's rb fitness, _geometrically_.
> This is why Hamilton et al had not other choice but
> to delete all genetic epistasis. It remained
> very convenient for Hamilton et al to agree with
> Fisher's dictate that stated epistasis is
> not heritable and therefore it remains
> non selectable so you can just forget
> about it. This contradicts
> _empirical_ evidence which has shown
> that within most genomes the vast
> majority of alleles at different loci
> are homozygous for exactly the same
> alleles. Sex shuffles the genes. If the
> card pack has over 90% the same cards
> then it matters little how much you
> shuffle the pack because most hands
> dealt will be almost same, i.e. most
> epistatic information is conserved and
> not lost.
But it would seem that your same card shuffling
argument would indicate that for loci which
have a nearly fixed allele homozygous, Hamilton
was doing no harm by deleting epistasis. It
doesn't matter if the "gene for altruism" needs
to partner epistatically with a gene at some
other locus in order to "work". Because there
is (almost) only one allele available in the
population at that locus, our "gene for altruism"
is (almost) certain to get the cooperation it
needs from the other locus.
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