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PALB2 chromatin recruitment restores homologous recombination in BRCA1-deficient cells depleted of 53BP1
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PALB2 chromatin recruitment restores homologous recombination in BRCA1-deficient cells depleted of 53BP1
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Journal Article
PALB2 chromatin recruitment restores homologous recombination in BRCA1-deficient cells depleted of 53BP1
2020
Overview
Loss of functional BRCA1 protein leads to defects in DNA double-strand break (DSB) repair by homologous recombination (HR) and renders cells hypersensitive to poly (ADP-ribose) polymerase (PARP) inhibitors used to treat BRCA1/2-deficient cancers. However, upon chronic treatment of BRCA1-mutant cells with PARP inhibitors, resistant clones can arise via several mechanisms, including loss of 53BP1 or its downstream co-factors. Defects in the 53BP1 axis partially restore the ability of a BRCA1-deficient cell to form RAD51 filaments at resected DSBs in a PALB2- and BRCA2-dependent manner, and thereby repair DSBs by HR. Here we show that depleting 53BP1 in BRCA1-null cells restores PALB2 accrual at resected DSBs. Moreover, we demonstrate that PALB2 DSB recruitment in BRCA1/53BP1-deficient cells is mediated by an interaction between PALB2’s chromatin associated motif (ChAM) and the nucleosome acidic patch region, which in 53BP1-expressing cells is bound by 53BP1’s ubiquitin-directed recruitment (UDR) domain.
Although loss of BRCA1 leads to defects in DNA double-strand break repair by homologous recombination (HR) and renders cells hypersensitive to PARP inhibitors, resistance to the drugs can arise. Here the authors reveal that PALB2 chromatin recruitment restores HR in BRCA1-deficient cells depleted of 53BP1.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/1
/ 13/106
/ 13/109
/ 13/89
/ 14/19
/ 14/35
/ 14/63
/ 38/22
/ 38/23
/ 42
/ 42/41
/ 42/70
/ 49/31
/ 82/16
/ 82/29
/ 82/80
/ 82/83
/ Defects
/ DNA
/ Fanconi Anemia Complementation Group N Protein - chemistry
/ Fanconi Anemia Complementation Group N Protein - deficiency
/ Fanconi Anemia Complementation Group N Protein - genetics
/ Fanconi Anemia Complementation Group N Protein - metabolism
/ Homology
/ Humanities and Social Sciences
/ Humans
/ Mutants
/ Repair
/ Ribose
/ Science
/ Tumor Suppressor p53-Binding Protein 1 - deficiency
/ Yeast
