An outstanding question in the evolution of aging is whether telomerase activity (which preserves the ends of linear chromosomes and lengthens the replicative lifespan of cells) is related to lifespan per se.
On on hand, it seems likely that it would be related positively: The longer one lives, the longer one’s cells need to continue regenerating. On the other hand, the longer one lives, the more likely one is to accumulate cells with oncogenic lesions. Since telomere maintenance is essential for tumor cell viability, one might not want these damaged cells to have ready access to telomerase expression…and this logic might lead us to the opposite conclusion.
A further confounding factor is body mass: In order to get a larger body, one needs more cell divisions, so one might expect larger organisms to exhibit higher telomerase activity. Then again…more cells means more risk of cancer…
It’s almost like one can’t derive biology from pure logic.
Coming down firmly on one side of the argument, Seluanov et al. show that among rodents, telomerase activity has co-evolved with body mass, but not lifespan. Furthermore, the correlation is negative: telomerase activity is more restricted in larger animals, perhaps as a defense against the increased cancer risk that comes from having more cells:
In multicellular organisms, telomerase is required to maintain telomere length in the germline but is dispensable in the soma. Mice, for example, express telomerase in somatic and germline tissues, while humans express telomerase almost exclusively in the germline. As a result, when telomeres of human somatic cells reach a critical length the cells enter irreversible growth arrest called replicative senescence. Replicative senescence is believed to be an anticancer mechanism that limits cell proliferation. The difference between mice and humans led to the hypothesis that repression of telomerase in somatic cells has evolved as a tumor-suppressor adaptation in large, long-lived organisms. We tested whether regulation of telomerase activity coevolves with lifespan and body mass using comparative analysis of 15 rodent species with highly diverse lifespans and body masses. Here we show that telomerase activity does not coevolve with lifespan but instead coevolves with body mass: larger rodents repress telomerase activity in somatic cells. These results suggest that large body mass presents a greater risk of cancer than long lifespan, and large animals evolve repression of telomerase activity to mitigate that risk.