Is this true?



Rick <[email protected]> wrote or quoted:
> Tim Tyler <[email protected]> wrote in message news:<[email protected]>...
> > Rick <[email protected]> wrote or quoted:
> > > Tim Tyler <[email protected]> wrote in message news:<[email protected]>...
> > > > Rick <[email protected]> wrote or quoted:

> I'm not trying to win points - just trying to understand.
>
> > Selection can tell which genes have been zapped - but to do that it has to grow them into a
> > whole organism and see how well they reproduce compared to their fellows - hardly a *simple*
> > process.
> >
> > I human watcher can sometimes tell whether a gene has been mutated by seeing if it codes for a
> > known useful protein - or comparing it with expected data - but again, this isn't a *simple*
> > process.
> >
> > It's true that - given two copies of a gene you can't /easily/ tell which one is the right one.
> >
> > Selection can tell, though - and a "backup copy" may well allow an organism with a mutation on
> > one bit of their Y chromosome to still be able to have some offspring without that mutation.
>
> In paired chromosomes there is a gene on each chromosome and somehow one is switched on and the
> other switched off. [...]

Sort of. Often both are translated into protein. Dominance and recessiveness is a consequence of the
resulting proteins on the organism. If one codes for something important - and the other is a
dysfunctional mess, then a double-dose of the latter might have dire consequences - which would have
been masked if there was a single copy of the good gene around. This is the "hallmark" of a
"recessive" gene.

> When I originally read the phrase "error correction mechanism" I thought it meant that the good
> gene would be dominant instead of the faulty gene or that when the Y-chromosome has recombination
> with itself it corrects the faulty gene. But you interpretted it as meaning that the faulty gene
> is weeded out by selection. I don't see why you haven't considered that error correction could
> happen in the Y-chromosome because if a correct gene can be chosen for dominancy then it could be
> chosen to correct an error on the other copy in the Y-chromosome. [...]

That seems more like "error hiding" than "error correction".

The error is still there - it's just its effect is mostly masked. It is not *completely* masked - if
another mutation happens in the remaining good copy of the gene, things go wrong.

FWIW, it's not yet clear to me whether the second copy of these "palindrome" genes is expressed at
all. It may not be - in which case, dominance may not be relevant at all.
--
__________
|im |yler http://timtyler.org/ [email protected] Remove lock to reply.
 
On Sat, 21 Feb 2004 19:24:43 +0000 (UTC), Tim Tyler <[email protected]> wrote: ... [snip] ...
>
>FWIW, it's not yet clear to me whether the second copy of these "palindrome" genes is expressed at
>all. It may not be - in which case, dominance may not be relevant at all.

FWIW, a Y palindrome sequence is not expressed; it is not translated into protein. It can
align/pair with the matching expressed gene sequence and exchange portions in a process
conceptually similiar to crossing-over but only the gene sequence itself is translated to protein.
On the other hand, if this exchange is extensive and occurring in mitosis, then maybe every portion
of the original palidrome, from the initial cell, would be now found in the gene sequence of some
cell and hense be expressed. How extensive this exchange and whether it occurs in mitosis is not
yet known. William L Hunt

>--
>__________
> |im |yler http://timtyler.org/ [email protected] Remove lock to reply.
 
[email protected] (Rick) writes:

> In Adam's Curse Brian Sykes says this:
>
> "Over the last hundred generations, going back to well before the birth of Christ, the
> mitochondria you got from your mother had experienced only 2,400 potentially risky cell divisions.
> Compare that to your Y-chromosome, if you have one, which has been copied about five hundred
> thousand times over the same period."
>
> This is one of the reasons why he claims that men are doomed in the next 100,000-200,000 years
> unless we evolve (naturally or articially) a new way of triggering men (instead of relying on the
> genes carried in the Y-chromosone).

I don't get it. 2400 cell divisions is good, 500,000 is bad, but 250,000 (the number divisions for
autosomes) is fine too?

--
Steve Schaffner [email protected] Immediate assurance is an excellent sign of probable lack of
insight into the topic. Josiah Royce
 
>> The second is that you're potentially losing a great
>> number of phenotypes during the mutation's lifetime in
>> the population due to either inviability or
>> noncompetitiveness. It is the amelioration of this effect
>> which is the primary drving force underlying the
>> evolution of error-correcting mechanisms.

>IMO, correcting deleterious errors is the primary drving
>force underlying the evolution of error-correcting
>mechanisms.

WA:- While you make the motions of trying to contradict what
I wrote, you are in fact writing precisely the same thing.
"Deleterious errors" are assessedsolely by the
competitiveness of the affected phenotypes within their
environment, vis-a-vis their competitor species. Ecological
competitiveness governs the evolved species genome, not the
other way around.

JE:- Proposed cause and effect are commonly but quietly
reversed within misused, oversimplified Neo Darwinian models
when discussion hots up. Hamilton's rule is a classic case.
Such action reduces most Neo Darwinian arguments to just a
Mad Hatter's Tea Party of contradiction. Prof. Felsenstein
had a solution: remove any reference to cause and effect
within the sciences. This is the same as curing a patient of
a terminal disease by killing the patent. Until discussion
of the proper use of models within Neo Darwinism is tackled
_openly_ and _fairly_, this absurd problem that plagues Neo
Darwinism must get worse.

John Edser Independent Researcher

PO Box 266 Church Pt NSW 2105 Australia

[email protected]
 
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