Reduced Rif2 and lack of Mec1 target short telomeres for elongation rather than double-strand break repair

Jean S. McGee, Jane A. Phillips, Angela Chan, Michelle Sabourin, Katrin Paeschke, Virginia A. Zakian

Research output: Contribution to journalArticle

52 Scopus citations

Abstract

Telomerase in Saccharomyces cerevisiae binds and preferentially elongates short telomeres, and this process requires the checkpoint kinase Tel1. Here we show that the Mre11 complex bound preferentially to short telomeres, which could explain the preferential binding of Tel1 to these ends. Compared to wild-type length telomeres, short telomeres generated by incomplete replication had low levels of the telomerase inhibitory protein Rif2. Moreover, in the absence of Rif2, Tel1 bound equally well to short and wild-type length telomeres, suggesting that low Rif2 content marks short telomeres for preferential elongation. In congenic strains, a double-strand break bound at least 140 times as much Mec1 in the first cell cycle after breakage as did a short telomere in the same time frame. Binding of replication protein A was also much lower at short telomeres. The absence of Mec1 at short telomeres could explain why they do not trigger a checkpoint-mediated cell-cycle arrest.

Original languageEnglish (US)
Pages (from-to)1438-1445
Number of pages8
JournalNature Structural and Molecular Biology
Volume17
Issue number12
DOIs
StatePublished - Dec 2010

All Science Journal Classification (ASJC) codes

  • Structural Biology
  • Molecular Biology

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