From: Robert Bradbury (bradbury@genebee.msu.su)
Date: Wed Jun 14 2000 - 07:54:00 MDT
On Tue, 13 Jun 2000, Joao Magalhaes wrote:
> Perhaps it's just me that am missing something but: if we can create
> embryonic stem cells from biopsies taken from old individuals, why should
> we care about preserving our cells while they're young?
To maximize the # of cells available with the minimum amount of accumulated
damage (with the implicit assumption that "damage" is accumulating.
> All the animal
> cloning experiments seem to show that the genome -- at least in some cells
> -- is perfectly preserved (although we still lack data for the longevity of
> clones, making this a provisionary, but probably accurate, statement).
All the cloning experiments show is that in the clones that *work*,
you have a "functional" genome. If the success rate is ~1% for
creating clones, that says there *may* be a lot of cells that cannot
create a functional organism. Miscarriage rates of 50-70% (rates
claimed vary) would argue this is true as well. The question is
whether the difference between 30-50% "good" germ cell "combinations"
and ~1% cloning success is due to even higher in vivo natural filtering
of defective cells (sperm/eggs) that isn't done in cloning, or is due to
real methodology problems in the clonning techniques.
> I know there is at least one company that does what you propose (they
> sent me some publicity a few months ago) but I really don't see the
> point in it.
The point would be as a backup strategy for individuals who are
pessimistic about the harvesting of stem-cells that can be grown
into organs as you grow older or who believe that whole genome
syn-cells or nanobot genome replacements are a long way away.
(Programmers try to look at all the possibilities.)
>
> On the same line of reasoning -- and I think I've posted a message about
> this before --, I'm still to ear a good explanation to the animal cloning
> experiments on the basis of the DNA damage theory of aging.
Some fraction of the genomes harvested being "good enough" is sufficent
explanation in my book.
> As for mitotic misregulation as the basis of aging, that's a speculatory
> conclusion. You can always argue that some upstream mechanism is regulating
> the genetic machinery and creating the mitotic imbalances.
>
Quite true, point mutations in any of the regulatory timing elements
coult through the whole thing into disarray.
Robert
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