HAATI survivors replace canonical telomeres with blocks of generic heterochromatin

Devanshi Jain, Anna K. Hebden, Toru M. Nakamura, Kyle M. Miller and Julia Promisel Cooper ()
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Devanshi Jain: Cancer Research UK, London Research Institute, 44 Lincoln’s Inn Fields, London WC2A 3PX, UK
Anna K. Hebden: Imperial College London Ovarian Cancer Action Group, London W12 0NN, UK
Toru M. Nakamura: University of Illinois
Kyle M. Miller: Gurdon Institute, Cambridge CB2 1QN, UK
Julia Promisel Cooper: Cancer Research UK, London Research Institute, 44 Lincoln’s Inn Fields, London WC2A 3PX, UK

Nature, 2010, vol. 467, issue 7312, 223-227

Abstract: Telomeres stabilized without telomerase The ends of eukaryotic chromosomes are composed of repeat sequences known as telomeres. Various proteins bind telomeres to protect them from degradation or inappropriate DNA repair responses, and their length is maintained by a specialized reverse transcriptase, telomerase. Jain et al. show that in the absence of telomerase, telomeres can be maintained by amplifying and recombining heterochromatin sequences there. This process requires histone methylation and two telomere-binding proteins, Pot1 and Ccq1. These findings suggest a mechanism by which cancer cells might escape the requirement for telomerase activation.

Date: 2010
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DOI: 10.1038/nature09374

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