Mail*Link( SMTP FWD>RE>"Reversing Human Aging" by M. Fossel
In reply to Todd Carter's comments "As i understand it, the
major hypothesis connecting telomerase with aging supposes that genes on
the distal regions of the chromosomes get "chewed up" as telomere length
reduces" it is important to realize that this is not quite right. This is
not the "major" theory. In fact, I don't know of anyone who is proposing
that in the literature. The hypothesis is really that loss of telomeric
repeats eventually leads to a chromosome end without repeats that "looks"
like a double strand break leading to DNA damage checkpoint arrest, or
alternatively, telomere shortening causes a shift of heterochromatin at
the telomere altering expression of telomeric genes. In support of the
former model, senescent cells have DNA damage-like alerations in cell
cycle regulators like p21, indeed it was first cloned there and called
"senescent derived inhibitor-1 (sdi-1)".
Therefore, cells approaching senescence have not lost essential genes (as
far anyone knows) and indeed recent results published in EMBO J suggest
that extending the telomeric repeats in hybrids results in an extension of
cell replicative lifespan.
-MWest
