From: Rafal Smigrodzki (rms2g@virginia.edu)
Date: Fri Dec 20 2002 - 08:48:09 MST
Joao wrote:
> Subject: RE: BIOLOGY: Mouse and Human Genome similarity
>
>
> Hi!
>
> At 11:02 10-12-2002 -0500, Rafal wrote:
>> ### Since toothy predators have been around for hundreds of millions
>> of years, one might expect that life should have found a way of
>> protecting itself from their depredations. The conclusion is that
>> tigers do not cause death.
>
> That is a ridiculous argument and it's easily disproved: tigers,
> unlike free radicals or UV, evolve. So when preys find a way to
> protect themselves against a predator, the predator also evolves. As
> far as I know, ultraviolet radiation, except perhaps now due to the
> Ozone problem, has remained constant for millions of years.
> Curiously, I remember reading about teeth evolution and how the teeth
> and jaws of modern animals have evolved so much since, say, the
> dinosaurs. So unlike the assumption in your argument, toothy
> predators have evolved a lot in the past hundreds of millions of
> years.
### Would you think that thanks to your having had an extra hundred million
years of evolutionary time behind your genes, you could easily deal with a
T.Rex? Whether you decide to call it "ridiculous", or not, it is a fact of
life that certain physical, chemical and information -management engineering
problems are hard, and evolution so far found no general solutions to them.
Just as organisms in general do not have a foolproof way of dealing with
teeth and claws, their ability to resist DNA damage is also limited.
Since in our ancestral environment teeth and claws were a much more
important factor than late-life accumulation of all kinds of DNA damage
(aneuploidy, chromosomal rearrangements, point mutations, mtDNA mutations,
dysmethylation, and other types of structural damage), we do have good
mechanisms (such as our brains and group organization) for dealing with the
former, but insufficient mechanisms for clearing the latter. I am sure you
are familiar with the argument that our ancestors hardly ever lived long
enough to need solutions to their late-life DNA damage problems - in this is
the answer why don't have them.
---------
>
> If you read my original message, I mentioned "bacterial culture", not
> "bacterial cell". Sure, individual cells are not immortal. Yet a
> bacterial culture, even when some cells suffer DNA mutations,
> survives. The question I ask is: why do we assume a multicellular
> organism can't cope with DNA damage? Why do we assume that DNA
> mutations accumulate in human cells when they don't in a bacterial
> culture? You can argue that non-dividing human cells can accumulate
> damage, but most cells in the body can be replenished by stem
> cells--even neurons.
### The answer is above - multicellular organisms under natural conditions
tend to die for all kinds of reasons (many of them toothy), and they need to
cope with DNA damage only long enough to cover their predicted lifespan.
Multicellular organisms deal with DNA damage but not well enough. The
complex web of adaptations necessary to prevent DNA damage longer than that
would have no chance to contribute to increased fitness, and therefore never
evolved in the first place.
Mutations do accumulate in bacterial cultures - if you propagate a strain
through many passages, you will be able to observe divergence from the
ancestral phenotype.
Stem cells accumulate damage, too. Replacing old and sick neurons with new
and sick neurons won't help.
-------
>> There is no doubt that DNA damage contributes to aging.
>
> I have doubts about everything we think we know about aging.
### Generally it's commendable to have doubts as a scientist, but at some
point the available evidence becomes simply too strong to leave room for
anything but the most general philosophic objections. The involvement of DNA
damage in aging is already at this level.
--------
>
> True, but--as I pointed to Robert, though probably off-list--you also
> need to go through hundreds of fetal cells to clone animals. Yet
> according to the theory, fetal cells should not have DNA mutations.
> My conclusion when both controls (i.e. fetal cells) and adult cells
> have a low chance of yielding viable cloned animals is that something
> is wrong in the process of cloning and not with the cells themselves.
> See the papers by Michael West and there's a few papers by a Korean
> team too.
### Yes, this is correct - we have insufficient knowledge of the processes
involved in cloning, so any conclusions either me or you could draw would be
of the highly conjectural type.
Rafal
This archive was generated by hypermail 2.1.5 : Wed Jan 15 2003 - 17:58:48 MST