The checkpoint clamp protein Rad9 facilitates DNA-end resection and prevents alternative non-homologous end joining

Feng Ling Tsai, Mihoko Kai

Research output: Contribution to journalArticlepeer-review

Abstract

DNA damage activates the cell cycle checkpoint to regulate cell cycle progression. The checkpoint clamp (Rad9- Hus1-Rad1 complex) is recruited to damage sites, and is required for checkpoint activation. While functions of the checkpoint clamp in checkpoint activation have been well studied, its functions in DNA repair regulation remain elusive. Here we show that Rad9 is required for efficient homologous recombination (HR), and facilitates DNA-end resection. The role of Rad9 in homologous recombination is independent of its function in checkpoint activation, and this function is important for preventing alternative non-homologous end joining (altNHEJ). These findings reveal novel function of the checkpoint clamp in HR.

Original languageEnglish (US)
Article number958386
Pages (from-to)3460-3464
Number of pages5
JournalCell Cycle
Volume13
Issue number21
DOIs
StatePublished - Nov 1 2014

Keywords

  • Cell cycle checkpoint
  • DNA repair
  • Homologous recombination

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology

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