Re: AGING: Accumulation of DNA damage

Date: Sat Jul 15 2000 - 10:39:41 MDT

> > >From: "Joao Pedro de Magalhaes" <>
>>>One thing that has always troubled me is: if non-coding regions are so easy
>>>to mutate and lose, how come they exist in such large amounts?

We have answers for the repetitive sequences. Dispersed repetitive DNA is
generally transposable and copies itself. Tandem repeats tend to expand
because of stutter during DNA replications. As to the non-repetitive stuff,
I don't know, although if specific duplications and deletions are relatively
comparable in rates, a given duplication may have a substantial transit
time before it gets deleted. Genome-wide, this could add up. writes:

> Though in writing this,
> I could see an advantage to decreased DNA if you had to develop
> faster (less copying of unrequired DNA means cell division can
> proceed more quickly).

This is the current accepted model for genome size, as I saw in
several presentations at the last evolution meeting. There are
good correlations between division rate and genome size.

> The reason I think, that there are so many non-coding regions,
> is because of the selective advantage (to the genes) for taking
> preexisting "working protein fragments" and inserting them
> into other genes. This is the work of the retrotransposons
> and is why we have so much junk DNA -- it speeds up the
> acceleration of evolution significantly beyond what simple
> mutations of individual bases will do.

They probably do speed evolution, but the primary reason they
exist is that they copy themselves. Presence of active transposons
is deleterious for the carriers; but the copy effect overcomes this.

> On Fri, 14 Jul 2000, phil osborn wrote:

> > Just a thought.. Suppose the introns, etc. are used for identification
> > purposes? Like a fingerprint. I wonder if they could figure into viral
> > defense?

Tandem duplications are used to align the chromosomes and function
as a "species fingerprint" of sorts. Introns proper are too short for
this most of the time. Parts of introns actually play roles in
splicing, and RNA editing, although probably not a large percent. Other
parts (considerably more) are selfish DNA. Most of it, though, has
no detectable excuse for existence, backing up the "accident" model.

Nobody has any models for introns defending against viruses although
a lot of transposons (=endogenous viruses) self-regulate by copy number.

This archive was generated by hypermail 2b29 : Mon Oct 02 2000 - 17:34:37 MDT