On Tue, 14 Dec 1999, Joao Pedro de Magalhaes wrote:
> I didn't know you were such a big fan of the telomerase theory!
Only in cells with a moderately high division rate, i.e. epithelial
(skin, lung, gut) cells, endothelial cells at high arterial stress
locations and perhaps T-cells (that might wear out with HIV
> However, the truth is that, unlike the free radical theory, the telomerase
> theory is a cellular, in vitro, theory, not an organismic one.
With respect to the collection of dividing cells (above), you could consider it to involve a substantial fraction of the organism. It depends whether we are talking about "aging" or "causes of death". In my original post, I was primarily talking about eliminating causes of death (sp. cancer). That may allow us to more fundamentally understand aspects of aging.
> Also, don't you think
> research based on Hayflick's limit (as most telomerase research is) can be
> biased? How do you explain that cells taken from species that appear not to
> age also follow Hayflick's limit and also have a latent period in
> accordance with donor age.
The question revolves around whether or not a cell *must* divide to not age. I could make the case that in mammalian species, there is an accumulation of metabolic byproducts (over very long time scales) that the cells do not know how to get rid of. The only way to prevent these from destroying cell functioning is to divide to dilute them down to a managable level. Now, a "non-aging species" may have mastered what is known to computer scientists as "garbage collection". In that case they would have no need to divide except to grow. Unless you have a clever genetic program to "grow" and "ungrow" very cleanly, growing indefinately might not be a good idea. At some point you exhaust the food resources, then cells start dying, then bacteria will come along to feed on the decayed material and they might start attacking the living material as well, etc.
So a non-aging species might have a "Hayflick limit" because exceeding your food resources makes you an invitation to creatures that might threaten your life.
> In addition, there is evidence indicating that
> telomerase is not the only enzyme controlling telomere lenght.
I'm unaware of this, but this might certainly be true. If the telomere length controlling mechanism is very old and the mammalian genome has been duplicated twice then there might be at least 4 paths controlling telomere length.
Cheers,
Robert