>`...another problem with the telomere hypothesis: Eggs are packed with
>enzymes that lengthen telomeres. [I assume she just means telomerase,
>that this is already in the cytoplasm of the host ovum. DB] In fact,
>of the first things eggs do when they are fertilized is to adjust the
>lengths of the telomeres on their chromosomes. So if a clone started out
>with telomeres that were too short, it is all but certain that the egg
>would lengthen them' (pp. 204-5).
>Okay, breathe easy for Dolly. But here's the kicker, something I haven't
>read anywhere else:
>`[Lee M.] Silver [of MOUSE GENETICS (OUP 1995) fame] told me that mouse
>researchers have even created mice that do not have [telomerase]. The
>seemed healthy... are now up their fourth generation [sans telomerase]...
>yet to find anything wrong...' (p. 205).
Yes, the telomerase "knockout" mice (to use the jargon) were perfectly
normal. They didn't even have increased rates of cancer, which I suppose
was unexpected. However, mice are not a good model for telomere research
because mouse cells can sometimes spontaneously immortalize in culture.
Human cells don't do that. Mice may have other ways of legthening their
telomeres other that telomerase.
The point you make about the ovum could be the crucial explanation of why
Dolly exists at all.
Tony Benjamin Csoka // Tel: (415) 476 2745 // Fax: (415) 476 9672