Hazel wrote:
> ... So mice really can't rely on telomere
> shortening to make their cells senesce, or else they would all be
> lumpy walking tumors and die faster
This is the traditional argument, but it's a bit oversimplified. In
principle, mice could quite well use telomere shortening to control
cell division after only ten or so more divisions than normal, which
would arrest tumours at a size of 1000 cells or so, which wouldn't
even kill a mouse. And indeed, as I mentioned earlier, mouse cells
really do enter senescence at about ten population doublings, though
very possibly not triggered by telomere shortening. The big problem
mice have, therefore, is that their cells escape from senescence (due,
presumably, to mutational events) extremely easily compared to human
cells, i.e. their senescence mechanism simply isn't very robust. (Of
course when I say "problem" I'm being anthropomorphic -- it would be
just as valid to say that mice can "afford" a mediocre senescence
mechanism because they only need to keep cancers at bay for a couple
of years.)
Aubrey de Grey