Re: Back in the good old days.

"William Morse" <wdNOSPAmorse@xxxxxxxxxxxxxxxx> wrote:
On Tue, 10 Feb 2009 18:28:34 -0500, Perplexed in Peoria wrote:

"John Harshman" <jharshman.diespamdie@xxxxxxxxxxx> wrote:
Perplexed in Peoria wrote:
"spintronic" <spintronic@xxxxxxxxxxx> wrote:
when spin argued against there being "Junk D.N.A".

There were a lot of big mouths on T.O claiming 95% of our genome was
Junk.

http://www.sciencedaily.com/releases/2008/11/081104180928.htm

Yep, there were, and I was one of them. This is a very interesting
article, Spin. Thx for posting the link. Here is the abstract
<http://genome.cshlp.org/content/18/11/1752> but unfortunately the
article itself requires a subscription.

I'm not sure whether this article really supports the belief that a
lot of that "95% junk" actually has a function. In discussing this,
it is important to first answer the question: "Cui bono?" Or,
"'Functioning' in whose interest?" Because what the "95%-ers" like me
have been saying all along is that all that 'junk' probably doesn't
serve a function for the organism that carries it. But we have always
conceded that much of the 'junk' is likely to be 'selfish DNA' - which
does nothing positive for the organism but does function for the
'benefit' of the DNA sequence itself. Transposons, for example.

But this article is suggesting that some of the junk has a function of
a different kind - a function benefiting a different entity. The
article claims that many binding sites for transcription factors got
to where they are today by riding on transposons. This is
interesting. Because people like me readily agree that the binding
sites of the transcription factors are functional for the organism,
and therefore not 'junk'. But we have been arguing that the
transposons are functional only for themselves, and hence are junk.
The article, however, argues that the transposons, by transporting the
transcription factor binding sites, have been acting to accelerate
evolution in various lines of mammals, and hence that they have a
function beyond their own selfish interests.

Well, yes they do, but if you look carefully, it cannot be called a
function which benefits the organism. The acceleration of evolution
is something which only shows a benefit in the long term, and as
Keynes tells us, in the long term the organism is dead. It seems that
the beneficiary of those 'junk' transposons would have to be an entity
with long term interests. I would say that the beneficiary is the
species (or deme). Conceivably, though, the beneficiary might be some
kind of Author of the evolutionary process. The "Author" has a
purpose in "Mind" for evolution - and arguably so does the species.
But the individual organism doesn't 'want' to evolve, and, in fact,
CAN'T evolve. So these evolution-enhancing transposons simply cannot
be said to serve a function for the benefit of the organism.
Therefore, I would say, they are still 'junk'.

Put more succintly, certain random mutations (of which transposon
insertions are one class) are occasionally beneficial, and so subject
to fixation by selection. If they benefit the organisms that contain
them, that is. I don't see where one gets an author (big or little a),
or even a benefit to the species, out of that.


Imagine you have a gene which (depending on which allele) turns a
particular class of mutations on or off. Is the 'on' allele beneficial
to the organism, and will it therefore increase in frequency in the
population?

Well, the answer to that question is going to depend on the properties
of that class of mutations. So, just so we have some definite numbers,
assume that the 'on' allele allows 1 mutation per generation, and that
the mutations are 90% neutral, 6% detrimental (s=0.1) and 4% beneficial
(also with s=0.1 (or should I say -0.1?) ).

So, it would seem that the 'on' allele does not benefit the individual
(on average) so it should be purged from the population. And simple
models which ignore genetic linkage endorse this conclusion. However, it
will occasionally happen that the 'on' allele will be closely linked
with one of the beneficial mutations which it permits. This complicates
the analysis.

AIUI, the result is going to depend on the details of the population
structure. It is a kind of group-selection problem. The 'on' allele is
an altruism gene. It produces benefits which eventually spread to the
entire population, but the carrier of this gene suffers detrimental
consequences which more than compensate.

Regardless of whether you yourself have the 'on' allele, it is to your
advantage if your neighbors have that alleles. Because if your neighbor
is unlucky and transmits a detrimental mutation to his offspring, that
offspring likely dies in childhood, doing you no harm. But if your
neighbor is lucky and transmits a beneficial mutation to his offspring,
that offspring reaches maturity and possibly breeds with your own
children.

To say it another way, in a sexual population, you want low fitness in
your pre-selection neighbors - because they are your competitors. But
you want high fitness in your post-selection neighbors - because your
grandchildren will share those genes.

So how to get low fitness pre-selection, but high fitness
post-selection? By having high variance in fitness (pre-selection). And
that is just what the 'on' allele accomplishes. It benefits the
population, though it slightly harms the individuals who bear it.

An intriguing argument. I don't know that I can adequately judge it
without a formal model that I probably wouldn't understand, but I can see
how this might work. I think your first example - the paragraph beginning
with 'Regardless" - is much more convincing than the pre-selection/post-
selection dichotomy.

It is a complicated argument, with many pieces - all essential. I need the
pre-selection/post-selection thing to explain why the guy carrying the
'on' gene (and hence some other mutations as well) gets a small net
detriment from the gene, since his descendents suffer those selective
deaths, but the deme-mates of the guy with the gene get a small net
benefit, because their descendents receive a disproportionate share
of the beneficial mutations (the detrimental mutations having been already
selected out by the time our original hero becomes an in-law.).

Possibly germane to this is the distinction made by Wilson and Holdobler
in "The Super-Organism", between the unit of selection and the target of
selection. The unit of selection they say is clearly the genome - this is
what changes under selection. The target of selection can be any of a
number of levels from the genome up to the species, depending on the
circumstances. Ordinarily the target of selection is the phenotype, but
it may be the kin group or could as in your case be the proximity group.
There appear to be other cases of proximity group selection as in
Mullerian mimicry.


"Proximity group". A nice piece of terminology I hadn't seen before.
I'll use it in the future. I see how it is exactly the right term for a concept
needed in the modeling of mimicry. I also see how it shows up in the
modeling of kin-selection-without-kin-recognition-altruism, since the
'proximity' group represents folks who benefit from each other's altruistic
actions.

But I don't think it applies to the argument I am making here. Because
the 'group' which benefits from a member's genetic 'R&D work' has more
to do with the local panmixis of mating patterns than it has to do with
physical proximity. I think I want the term Harshman suggested - 'deme'.

.

Relevant Pages

  • Re: Back in the good old days.
    ... a lot of that "95% junk" actually has a function. ... Put more succintly, certain random mutations are occasionally beneficial, and so subject to fixation by selection. ... Imagine you have a gene which (depending on which allele) turns ... But you want high fitness in your post-selection ...
    (talk.origins)
  • Re: Back in the good old days.
    ... a lot of that "95% junk" actually has a function. ... Imagine you have a gene which (depending on which allele) turns ... But you want high fitness in your post-selection ... You have the group selection changing directions between generations, ...
    (talk.origins)
  • Re: Back in the good old days.
    ... a lot of that "95% junk" actually has a function. ... doesn't serve a function for the organism that carries it. ... Put more succintly, certain random mutations are occasionally beneficial, and so subject to fixation by selection. ... Imagine you have a gene which (depending on which allele) turns ...
    (talk.origins)
  • Re: Back in the good old days.
    ... lot of that "95% junk" actually has a function. ... serve a function for the organism that carries it. ... to fixation by selection. ... Is the 'on' allele beneficial ...
    (talk.origins)
  • Re: Back in the good old days.
    ... a lot of that "95% junk" actually has a function. ... doesn't serve a function for the organism that carries it. ... certain random mutations (of which transposon ... Imagine you have a gene which (depending on which allele) turns ...
    (talk.origins)
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