Two replication fork remodeling pathways generate nuclease substrates for distinct fork protection factors.
Two replication fork remodeling pathways generate nuclease substrates for distinct fork protection factors.
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DOI：
10.1126/sciadv.abc3598
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发表时间：
2020-11
期刊：
影响因子：
13.6
通讯作者：
Cortez D
中科院分区：
文献类型：
--
作者：
Liu W;Krishnamoorthy A;Zhao R;Cortez D
At least two groups of fork protection factors work downstream of two RAD51-dependent fork remodeling pathways. Fork reversal is a common response to replication stress, but it generates a DNA end that is susceptible to degradation. Many fork protection factors block degradation, but how they work remains unclear. Here, we find that 53BP1 protects forks from DNA2-mediated degradation in a cell type–specific manner. Fork protection by 53BP1 reduces S-phase DNA damage and hypersensitivity to replication stress. Unlike BRCA2, FANCD2, and ABRO1 that protect reversed forks generated by SMARCAL1, ZRANB3, and HLTF, 53BP1 protects forks remodeled by FBH1. This property is shared by the fork protection factors FANCA, FANCC, FANCG, BOD1L, and VHL. RAD51 is required to generate the resection substrate in all cases. Unexpectedly, BRCA2 is also required for fork degradation in the FBH1 pathway or when RAD51 activity is partially compromised. We conclude that there are multiple fork protection mechanisms that operate downstream of at least two RAD51-dependent fork remodeling pathways.
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影响因子：
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通讯作者：
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