Telomeres avoid end detection by severing the checkpoint signal transduction pathway

Tiago Carneiro, Lyne Khair, Clara C. Reis, Vanessa Borges, Bettina A. Moser, Toru M. Nakamura and Miguel Godinho Ferreira ()
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Tiago Carneiro: Instituto Gulbenkian de Ciência
Lyne Khair: University of Illinois
Clara C. Reis: Instituto Gulbenkian de Ciência
Vanessa Borges: Instituto Gulbenkian de Ciência
Bettina A. Moser: University of Illinois
Toru M. Nakamura: University of Illinois
Miguel Godinho Ferreira: Instituto Gulbenkian de Ciência

Nature, 2010, vol. 467, issue 7312, 228-232

Abstract: How telomeres evade erroneous 'repair' The ends of chromosomes, known as telomeres, present a challenge to the cell — they look like an end generated by a double-strand break, but if treated as such, the DNA damage-repair system would initiate a checkpoint response and cause telomere–telomere fusions. Carneiro et al. now show that telomeres lack two types of histone modification that are required for recruitment of Crb253BP1, and that without Crb253BP1, even if other DNA damage-response proteins are recruited to a Taz1-deficient telomere, the checkpoint cannot be activated. These histone modifications are dependent on two telomere-binding proteins, Pot1 and Ccq1.

Date: 2010
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DOI: 10.1038/nature09353

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