Format

Send to:

Choose Destination
See comment in PubMed Commons below
Cell Cycle. 2007 May 15;6(10):1161-7. Epub 2007 May 30.

The cell division cycle puts up with unprotected telomeres: cell cycle regulated telomere uncapping as a means to achieve telomere homeostasis.

Author information

  • 1Department of Microbiology, Faculty of Medicine, Universit√©, de Sherbrooke, Sherbrooke, Quebec, Canada.

Abstract

Telomeres have unique properties that distinguish natural chromosomal ends from accidental DNA double-strand interruptions arising elsewhere in the genome. However, the slightest perturbation in their unique organization may obliterate this distinction, channelling chromosomal ends into unwarranted repair events, eventually causing genome instability. Recent results revealed that the processing of both dysfunctional telomeres and accidental DNA double strand breaks (DSB) by DNA repair activities is tightly regulated in a cell cycle-dependent manner by the S phase-promoting cell cycle kinase CDK1 (Clb-Cdc28p). Surprisingly, the cell cycle determinants and the timing of processing at unprotected telomeres closely match the requirements of other transactions that occur at telomeres. In particular, the replenishment of telomeric repeats by telomerase is tightly linked to cell cycle progression and occurs in the same interval. Furthermore, cell survival in the absence of essential telomeric proteins being dependent on telomere-telomere recombination mechanisms may require a similar regulation. Thus, a temporally limited state of telomere dysfunction leading to chromosome end processing may represent a well-governed cell cycle event that constitutes an integral part of the assembly of a new functional telomere.

PMID:
17495544
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Loading ...
    Write to the Help Desk