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Senescence: back to telomeres

Nature Reviews Molecular Cell Biology volume 14, page 196 (2013)Cite this article

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Nearly 50 years ago, Leonard Hayflick first described cellular senescence, a phenomenon now seen as an important suppressor of tumorigenesis. The term senescence was used to refer to an irreversible growth arrest that ensues after a fixed number of cell divisions, thereby marking the end of the proliferative lifespan of a cell. The underlying cause of senescence was subsequently ascribed to erosion of telomeres — nucleoprotein structures that protect natural chromosome ends from being recognized as broken DNA. As telomeres progressively shorten with every cell division, natural chromosome ends eventually lose telomere protection, are recognized as DNA damage and trigger senescence.

senescence ... can also arise within a few rounds of replication after the expression of an activated oncogene

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References

ORIGINAL RESEARCH PAPER

  1. Serrano, M. et al. Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a. Cell 88, 593–602 (1997)

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FURTHER READINGS

  1. Fumagalli, M. et al. Telomeric DNA damage is irreparable and causes persistent DNA-damage-response activation. Nature Cell Biol. 14, 355–365 (2012)

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  2. Hewitt, G. et al. Telomeres are favoured targets of a persistent DNA damage response in ageing and stress-induced senescence. Nature Commun. 3, 708 (2012)

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Authors and Affiliations

  1. The Netherlands Cancer Institute, Plesmanlaan 121, Amsterdam, 1066 CX, The Netherlands

    Jacqueline J. L. Jacobs

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  1. Jacqueline J. L. Jacobs
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Jacobs, J. Senescence: back to telomeres. Nat Rev Mol Cell Biol 14, 196 (2013). https://doi.org/10.1038/nrm3544

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