Review

  • The EMBO Journal (2009) 28, 2174 - 2187
  • doi:10.1038/emboj.2009.176

Published online: 23 July 2009

Taming the tiger by the tail: modulation of DNA damage responses by telomeresEMBO Open

David Lydall1

  1. Centre for Integrated Systems Biology of Ageing and Nutrition, Institute for Ageing and Health and Institute of Cell and Molecular Biosciences, Newcastle University, Tyne and Wear, UK

Correspondence to:

David Lydall, Institute for Ageing and Health, Newcastle University, Henry Wellcome Laboratory, Newcastle upon Tyne, Tyne and Wear, NE4 5PL, UK. Tel.: +44 191 248 1207; Fax: +44 191 248 1101; E-mail: D.A.Lydall@ncl.ac.uk

Received 14 April 2009; Accepted 3 June 2009


Telomeres are by definition stable and inert chromosome ends, whereas internal chromosome breaks are potent stimulators of the DNA damage response (DDR). Telomeres do not, as might be expected, exclude DDR proteins from chromosome ends but instead engage with many DDR proteins. However, the most powerful DDRs, those that might induce chromosome fusion or cell-cycle arrest, are inhibited at telomeres. In budding yeast, many DDR proteins that accumulate most rapidly at double strand breaks (DSBs), have important functions in physiological telomere maintenance, whereas DDR proteins that arrive later tend to have less important functions. Considerable diversity in telomere structure has evolved in different organisms and, perhaps reflecting this diversity, different DDR proteins seem to have distinct roles in telomere physiology in different organisms. Drawing principally on studies in simple model organisms such as budding yeast, in which many fundamental aspects of the DDR and telomere biology have been established; current views on how telomeres harness aspects of DDR pathways to maintain telomere stability and permit cell-cycle division are discussed.

  • Keywords:

    • checkpoint,
    • DNA-damage response,
    • telomere

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits distribution, and reproduction in any medium, provided the original author and source are credited. This license does not permit commercial exploitation or the creation of derivative works without specific permission.

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