PARP1 and PARP2 stabilise replication forks at base excision repair intermediates through Fbh1-dependent Rad51 regulation.

regulates the repair of DNA single-strand breaks generated directly, or during base excision repair (BER). However, the role of in these and other repair mechanisms is unknown. Here, we report a requirement for Pduanyu372 in stabilising replication forks that encounter BER intermediates through Fbh1-dependent regulation of Rad51. Whereas Pduanyu372 is dispensable for tolerance of cells to SSBs or homologous recombination dysfunction, it is redundant with Pduanyu371 in BER. Therefore, combined disruption of Pduanyu371 and Pduanyu372 leads to defective BER, resulting in elevated levels of replication-associated DNA damage owing to an inability to stabilise Rad51 at damaged replication forks and prevent uncontrolled DNA resection. Together, our results demonstrate how Pduanyu371 and Pduanyu372 regulate two independent, but intrinsically linked aspects of DNA base damage tolerance by promoting BER directly, and by stabilising replication forks that encounter BER intermediates.

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