Affiliation:
1. Department of Molecular Microbiology and Biotechnology, Tel Aviv University, Ramat Aviv 69978, Israel
Abstract
ABSTRACT
Upon chromosomal damage, cells activate a checkpoint response that includes cell cycle arrest and a stimulation of DNA repair. The checkpoint protein Rad24 is key to the survival of a single, repairable double-strand break (DSB). However, the low survival of
rad24
cells is not due to their inability to arrest cell cycle progression. In
rad24
mutants, processing of the broken ends is delayed and protracted, resulting in extended kinetics of DSB repair and in cell death. The limited resection of
rad24
mutants also affects recombination partner choice by a mechanism dependent on the length of the interacting homologous donor sequences. Unexpectedly,
rad24
cells with a DSB eventually accumulate and die at the G
2
/M phase of the cell cycle. This arrest depends on the spindle checkpoint protein Mad2.
Publisher
American Society for Microbiology
Subject
Cell Biology,Molecular Biology
Cited by
61 articles.
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