>The problem for "aging gene" theory is not so much the wide effects
>of aging as the variability.
What variability? I said before that there are great similarities in the
aging process of all well-studied mammals.
I've got another question, why don't reptilians or amphibians show
widespread aging? Even species such as Desmognathus that live less than 15
years do not show signs of increased mortality with age (in fact, they show
decreased mortality after adulthood is reached). So, how come some species
-- e.g. mammals -- accumulate all those thousands of genes causing
age-related changes you claim to exist and others accumulate none? According
to your evolutionary theory, all species should be on equal grounds to
accumulate age-related pathologies; the only factor would be mortality (and
subsequent longevity); but that alone does not explain why is aging present
in all known species of a class and practically none of others.
>No, two genetic effects which produce many but not all aging phenotypes
>don't prove that you can't produce those phenotypes by other mechanisms.
>Indeed, every inbred mouse line seems to have a different way to get
I'm not saying helicases cause aging. I'm just saying that they control many
age-related pathologies, disproving your theory that age-related pathologies
are caused by independant genes. As to what are the true timekeepers of
aging, that is pure speculation.
Joao Pedro de Magalhaes
The University of Namur (FUNDP)
Unit of Cellular Biochemistry & Biology
Rue de Bruxelles, 61
B-5000 Namur BELGIUM
Fax: + 32 81 724135
Phone: + 32 81 724133
Reason's Triumph: http://users.compaqnet.be/jpnitya/
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