gwmartin at husc8.harvard.edu
Wed Apr 27 08:34:05 EST 1994
Sydney Shall (bafa1 at central.susx.ac.uk) wrote:
: The enzyme telomerase has been shown to be present in immortal
: cell lines. However, it has never been purified and therefore it has
: never been cloned.
Yeast telomeres were first cloned in 1982 (Szostak & Blackburn; Cell
29:245). Tetrahymena telomerase was cloned in 1987
(Greider & Blackburn; Cell 51: 887) and I suspect a mammalian homologue
has since been cloned. Telomerase turns out to be a protein which contains
a small RNA molecule, used to prime telomere synthesis.
: The average length of telomeres in dividing normal,
: untransformed cells has been shown to shorten as the cell culture ages.
True. And Lundblad & Szostak (1989) showed that in yeast, defects in
telomere elongation correlates with senescence.
: That is, there is a correlation between the length of the average
: telomere size and the age of the culture.
: The predictions of what the re-introduction of a telomerase
: enzyme might do in ageing cells requires the cloning of the gene for
: this enzyme. This is proving a very difficult task.
: In presence it should be possible to reactivate the expression
: of this gene in normal cells, and to repress its expression in cancer
: cells, but this also awaits the cloning of the gene.
But, only actively dividing cells would really have a need for
telomerase, right? I don't know how many cell types, besides epithelial
and hematopoietic cells, aren't terminally differentiated in adults.
However, part of the problem with transformed cells is that they do not
senesce (sp?), like you imply. But I wonder if maintenace of telomere
integrity isn't part of some greater cellular aging program. In that
case, turning on telomerase in cancer cells may not have the desired effect.
: This area is therefore both very active and very excitibg, and
: there is lots of room for more people in this field.
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