Abraxas suppresses DNA end resection and limits break-induced replication by controlling SLX4/MUS81 chromatin loading in response to TOP1 inhibitor-induced DNA damage

Abstract

Break-induced replication (BIR), a subtype of HR, is a mutagenic mechanism that leads to chromosome rearrangements. Here the authors reveal insights into the role of Abraxas in limiting excessive DNA end resection, R-loop accumulation and cells undergoing BIR-dependent mitotic DNA synthesis.