An Anti-Checkpoint Activity for Rif1

Yaniv Harari,Linda Rubinstein,Martin Kupiec,Sue Biggins

doi:10.1371/journal.pgen.1002421

Abstract

An Anti-Checkpoint Activity for Rif1

Highlights

Chromosomal double-strand breaks (DSBs) are among the most severe lesions a cell has to deal with: if left unrepaired, they may lead to cell death or cancer
The presence of Rif1 had a negative effect on the recruitment of the checkpoint sensors Replication Protein A (RPA), Ddc2ATRIP, Ddc1RAD9, and Rad953BP1: a much higher recruitment of these proteins was seen in strains lacking Rif1 than in the wild type
With time after temperature shift, the negative effect of Rif1 was stronger at proximal sites than at the subtelomeric sequences, suggesting that the Rif1 protein itself moves; these effects were not caused by increased single-stranded DNA (ssDNA) levels or by changes in the dynamics of resection

Summary

Introduction

Chromosomal double-strand breaks (DSBs) are among the most severe lesions a cell has to deal with: if left unrepaired, they may lead to cell death or cancer. The Rif1 and Rif2 proteins seem to have important, yet different, roles in determining the integrity and length of telomeres [4,5,6]. Xue and co-workers [2] have studied the recruitment of several proteins to the telomeres in a strain carrying the temperature-sensitive cdc13-1 allele.

Results

Conclusion