Logo image
Break Induced Replication: the where, the why, and the how
Journal article   Open access   Peer reviewed

Break Induced Replication: the where, the why, and the how

J Kramara, B Osia and A Malkova
Trends in genetics, Vol.34(7), pp.518-531
07/2018
DOI: 10.1016/j.tig.2018.04.002
PMCID: PMC6469874
PMID: 29735283
url
https://doi.org/10.1016/j.tig.2018.04.002View
Published (Version of record) Open Access

Abstract

Break induced replication (BIR) is a pathway that repairs one-ended double strand breaks (DSBs). For decades, yeast model systems offered the only opportunities to study eukaryotic BIR. These studies described an unusual mode of BIR synthesis that is carried out by a migrating bubble and shows conservative inheritance of newly synthesized DNA, leading to genomic instabilities like those associated with cancer in humans. Yet, evidence of BIR functioning in mammals or during repair of other DNA breaks has been missing. Recent studies have uncovered multiple examples of BIR working in replication restart and repair of eroded telomeres in yeast and mammals as well as some unexpected findings, including the RAD51 independence of BIR. Strong interest remains in determining the variations in molecular mechanisms that drive and regulate BIR in different genetic backgrounds, across organisms, and particularly in the context of human disease.
alternative lengthening of telomeres break-induced replication MMBIR mutation cluster Rad51-dependent BIR RAD51-independent BIR

Details

Metrics

Logo image