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Reply to “Telomere-dependent senescence”

Nature Biotechnology volume 17, pages 313–314 (1999)Cite this article

Harry Rubin replies:

The authors and cosigners of the two letters1,2 responding to my several critiques on cellular aging3,4,5,6 have consistently ignored the main thrust of that critique, which is that primary fibroblasts senesce in culture in a stochastic manner rather than with a uniform, genetically fixed lifespan. Half of the clones undergo 16 divisions or less7,8, rather than the uniform 50 for all the cells usually quoted in the senescence literature. The products of a single mitosis may differ widely in replicative lifespan9. Random genetic damage certainly fits better with that picture than does a telomere clock. Indefinite division, which is characteristic of established cell lines, does not mean that cells are not dying; it means that replication in a population outstrips death.

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  1. University of California, Berkeley

    Harry Rubin

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Rubin, H. Reply to “Telomere-dependent senescence”. Nat Biotechnol 17, 313–314 (1999). https://doi.org/10.1038/7829

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