Genome-wide screen reveals dependence of break induced replication on several distinct checkpoints.

ABSTRACT: Break-induced replication (BIR) is a primary homologous recombination pathway for repairing one-ended double-strand DNA breaks, including those arising from collapsed replication forks and eroded telomeres. BIR frequently leads to loss of heterozygosity, genetic mutations, and gross chromosomal rearrangements, all hallmarks of cancer. Here, we conducted a genome-wide screen that allowed us to identify and validate the involvement of 33 novel yeast genes in BIR. We report that, while DNA damage and spindle checkpoint machineries are both required to delay nuclear division and provide adequate time for BIR to complete, the spindle position checkpoint is required to coordinate between nuclear division and cytokinesis. Furthermore, we show that two nucleopore proteins play a sequential role du

SUBMITTER: Liu L 

PROVIDER: S-EPMC12804954 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature