>>why do we die

Ron Grunwald grun at acpub.duke.edu
Fri Nov 3 20:37:45 EST 1995

sb008c at uhura.cc.rochester.edu (Seth Bordenstein) wrote:

>   Why do we die? In order to understand why we die, we need to understand
> why we age; And this has something to do with a relative decrease in
> Telomerase concentrations. Telomerase is the enzyme which recognizes a
> certain sequence repeat at the end of chromosomes. It consequently adds base
> pairs in an unusual structure that may act as a protective structure of the
> chromosome ends.  As telomerase concentrations decrease over time, more of
> our chromosome ends lose the protective structure and pieces get degraded.
> Chromosome ends get chopped off, DNA is lossed, and you begin to age....
> Seth Bordenstein
> sb008c at uhura.cc.rochester.edu

While the absence of telomerase activity undoubtedly contributes to the
mechanism of senescence, it doesn't address the evolutionary question of
why we die. The loss of telomerase activity in most somatic cells is not
some inevitable consequence of a system breaking down but is, instead, a
regulated behavior of the cell. 

The expression of telomerase is repressed in most terminally
differentiated cells, with the notable exception of germ line cells.
Telomerase expression in differentiated cells can be upregulated as it is
in immortalized cancer cells. The repression of telomerase activity
therefore appears to be the result of selection for limiting the lifespan
of most somatic cell lines. 

It is also worth noting that in the abscence of telomerase individual
cells that continue to replicate are confronted fairly quickly (~20-30
generations? there is a recent Science article on this) with a chromosome
crisis that triggers apoptosis (regulated cell suicide). So I don't think
that senescence of the organism is easily pinned on the direct cellular
consequences of loss of telomeres.

While death may be an inevitable consequence of being an error prone
system, the actual lifespan of a organisms is indeed an evolved trait
refelcting primarily the level of DNA repair as well as telomerase. The
question posed in this thread then returns to what is the selective
advantage of limiting the lifespan of an individual.

Ron Grunwald                             

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