On Mon, 1 May 2000, Joao Pedro de Magalhaes wrote:
> I believe -- can't find the reference -- some Asian scientists cloning mice
> did find a correlation between donor age of the nucleus and the chances of
> creating a viable clone.
That would be a useful bit of information. What would be *very* interesting
would be to compare clones produced from normally dividing cells, such
as intestinal cells as I believe was the case with Dolly, cells with
replicative potential (liver), and non-dividing cells (neurons, muscle, ???).
The question is whether the non-dividing cell can be dedifferentated
back to a dividing state. If you could do that, then you could use
cells from young, middle-aged & old animals and really get a handle
on the degree to which mutation accumulation damages genome integrity.
> John K Clark wrote:
> > That's even more direct evidence. I grant you it still doesn't prove the
> > entire animal will live longer but it does give considerable weight to
> > that idea; and a increase from 61 to 93 divisions is not small and is not
> > theoretical, it's a concrete experimental result.
> Mice having shorter telomeres at birth do not live less than controls. There
> is no correlation between in vitro doubling potential from cells taken
> post-partum and life span. Therefore it is unlikely that we will witness a
> 50% or close increase in the life span in these animals. I personaly am more
> interested in seeing the results from Blasco's knock in telomerase mice.
Joao, you may know the answer to this. Wasn't there a report
(perhaps from Univ. of Hawaii?) that telomerase knockout mice *do*
show signs of inability to develop and/or accelerated aging after
3-4 generations? If that is true, it might suggest that normal
telomere lengths in adults would be sufficient to develop 2nd
generation and perhaps even 3rd generation organs from stem cells
remaining in the adult body, *without* the necessity of lengthening
the telomeres through cloning or other processes. Presumably
more terminally differentiated cells (that have gone through
more cell divisions) would be a poorer source material due
to shorter telomeres, *if* you could regress them to a
stem cell state. Now, given the shorter telomeres in humans
it would be unclear whether the stem cells in adult humans
could be used to grow replacement organs.
What we need is the # of cell generations required to produce
a 3-5 kg organ from a single cell, the normal adult human telomere
length and how much each cell division subtracts from the telomeres.
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