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Telomeres avoid end detection by severing the checkpoint signal transduction pathway

Author

Listed:
  • 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)

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.

Suggested Citation

  • Tiago Carneiro & Lyne Khair & Clara C. Reis & Vanessa Borges & Bettina A. Moser & Toru M. Nakamura & Miguel Godinho Ferreira, 2010. "Telomeres avoid end detection by severing the checkpoint signal transduction pathway," Nature, Nature, vol. 467(7312), pages 228-232, September.
    • Handle: RePEc:nat:nature:v:467:y:2010:i:7312:d:10.1038_nature09353
    DOI: 10.1038/nature09353
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