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.
Jean-Pierre Issa wrote:
>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
I may be wrong but what I think jim and barbara burkhart were
reffering to was the aspect that imprinting can play in
development... I don't think all DNA Methylation patterns are
removed following miosis - the damaged gene which causes
Angelman syndrome in females ,(I think!) is the same as that
which causes Prauder-Willie (spelling?) syndrome...
I may well be wrong (as my memory is not the best) but the differences
in phenotype are determined by whether the gene is inhereted from
the father or the mother..(via I think differences in parent methylation
patterns.
I could well be wrong but I think there are other cases (such as an
offspring inheriting for eg. two chromosome 11's from the father and
none from the mother) where the offsprings phenotype is affected(?)
The second possibility is that I am talking complete b****ks..
I would be interested if anyone out there could make some sense
of this post and the relevance of methylation/demethylation in
embryogenisis vs aging?
Cheers!
Gary Morley
gmorley at rpms.ac.uk
