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. 2022 Mar 1;36(5-6):278–293. doi: 10.1101/gad.349431.122

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© 2022 Hopkins et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 2. — Functions of BRCA1/2 in protecting replication forks. In BRCA1/2-proficient cells, reversed replication forks are protected from nucleolytic degradation by RAD51 in a BRCA1/2-dependent manner. In BRCA1/2-deficient cells, nascent DNA at reversed forks is increasingly degraded. Degradation of nascent DNA in BRCA2-deficient cells leads to MUS81- and POLD3-dependent, error-prone fork restart. Furthermore, ssDNA gaps accumulate during replication in BRCA1/2-deficient cells. BRCA1-deficient cells are defective for protecting ssDNA gaps against the MRE11 nuclease, reducing TS- and TLS-mediated gap repair.