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smc smc at
Tue Mar 10 13:41:54 EST 1998

On Mon, 09 Mar 1998 22:04:33 -0600, Iuval Clejan <spring at> wrote:

>As far as I understand, all human cells with nuclei come from precursor cells which do indeed 
>divide, with a few exceptions such as cells in the nervous system. This must be true even for 
>the adult human, otherwise wounds would not heal. I see no reason why adult C. Elegans would not 
>have cells which undergo division. CE, along with other organisms, probably slow down the rate 
>of cell division (under normal circumstances) with age. I can't remember now if someone found 
>a correlation of telomere length with age in humans. Perhaps it was only the number of 
>divisions till the Hayflick limit in vitro that correlates with age(?)Please let me know if I'm 

In fact there is both an inverse correlation between telomere length and the age
of the organism (across almost every species tested), as well as telomere length
and in vitro cell population doublings (the Hayflick limit). To add to the
evidence of the involvement of telomeres in ageing there is also evidence for a
positive correlation between telomere length and the mean lifespan of a species,
except for a few strange cases such as the mouse which has disproportionately
long telomeres. However it is likely that it is not only telomere length that
determines the Hayflick limit of cells, but also the rate of telomere loss
during each mitotic division.

Regarding C. elegans, I'm pretty certain all its cells are post-mitotic and so
are not replaced. However, CE still ages and dies, as do all post-mitotic cells
(e.g. neurons), and so this is where the involvement of telomeres and telomerase
in ageing becomes uncertain. My best bet is that telomeres are simply an
anti-cancer mechanism inhibiting the number of times a cell can replicate,
especially since the telomers of humans who have died of old age are still quite
long and go on dividing in vitro (albeit fewer times than a young person). 


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