I disagree with your dismissal of methylation's role in
aging: DNA methylation patterns are reset during early
embryogenesis. In fact, the Dolly experiment supports a
methylation theory of aging (changes irreversible in adult
cells but reversible in embryonal cells) over a mutational
theory of aging (changes irreversible no matter what).
Incidentally, there is some data suggesting that this may be
true for some cancers as well.
Jean-Pierre Issa
grendle at worldnet.att.net (jim and barbara burkhart) wrote:
>The cloning of the sheep has certainly opened a number of questions
>about the regulation of lifespan and the critical aging signal. The
>possibilty importance of methylation was mentioned. Alternate
>methylation patterns in maternal and paternal gametes have been
>suggested as critical for development but the cloning of the sheep
>clearly doesn't require gamete methylation programing. The suggestion of
>methylation as important to ageing is likewise defeated by the sheep. In
>both cases the presumed crucial methylation is a property of the "old"
>nucleus but development apparently proceeds normally. I believe that
>implicates the programming of the egg as critical.
>Does the ageing signal reside in the nucleus? If the ageing "clock" is
>nuclear, DNA damage or telomere lenth have been proposed, then Dolly is
>a problem. Perhaps the successful fusion contains not the odd undamaged
>nucleus but a nucleus that has lost genes critical to sensing ageing. It
>will be interesting to see if clones have an elevated cancer incidence.
