Ring Finger Nuclear Factor RNF168 Is Important for Defects in Homologous Recombination Caused by Loss of the Breast Cancer Susceptibility Factor BRCA1

Muñoz, Meilen C.; Laulier, Corentin; Gunn, Amanda; Cheng, Anita; Robbiani, Davide F.; Nussenzweig, André; Stark, Jeremy M.

doi:10.1074/jbc.m112.410951

Cited by 45 publications

(47 citation statements)

References 57 publications

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“…Thus, factors that regulate the extent of resection likely cause differential effects on these pathways. Consistent with this notion, the DNA damage response pathway involving the end resection inhibitor 53BP1 appears important for the balance of repair in favor of HDR versus SSA [14, 19, 110]. …”

Section: Cellular Contexts That May Favor Ssa Versus Other Repair Eventsmentioning

confidence: 92%

“…For example, SSA is dependent on CtIP [14, 15], which is a key end resection factor, based on cell biology measurements of ssDNA formation at sites of DNA damage, as well as physical analysis of site-specific endonuclease-generated chromosomal DSBs [16–18]. Conversely, factors that inhibit end resection have been found to suppress SSA, such as the DNA damage response pathway involving H2AX, RNF168, 53BP1, and RIF1 [14, 18–21]. Beyond these examples, numerous other factors that promote/inhibit end resection have a corresponding effect on SSA [22–37].…”

Section: Chromosomal Break Repair By the Single Strand Annealing (Ssamentioning

confidence: 99%

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Regulation of Single-Strand Annealing and its Role in Genome Maintenance

2016

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Single Strand Annealing (SSA) is a DNA double strand break (DSB) repair pathway that uses homologous repeats to bridge DSB ends. SSA involving repeats that flank a single DSB causes a deletion rearrangement between the repeats, and hence is relatively mutagenic. Nevertheless, this pathway is conserved, in that SSA events have been found in several organisms. In this review, we describe the mechanism of SSA and its regulation, including the cellular conditions that may favor SSA versus other DSB repair events. We will also evaluate the potential contribution of SSA to cancer-associated genome rearrangements, and to DSB-induced gene targeting.

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Section: Cellular Contexts That May Favor Ssa Versus Other Repair Eventsmentioning

confidence: 92%

Section: Chromosomal Break Repair By the Single Strand Annealing (Ssamentioning

confidence: 99%

Regulation of Single-Strand Annealing and its Role in Genome Maintenance

2016

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“…To knock down genes in U2OS cells, the following small interfering RNAs (siRNAs) were used: siNC (siRNA universal negative control 1) (SIC001; Sigma-Aldrich), siCdc14A (SASI_Hs01_00132334; Sigma-Aldrich), siCdc14B (GAGCAGCCUUCUCCAAACUdTdT) (16), siBRCA1 (GGGAUACCAUGCAACAUAAdTdT) (17), and si53BP1 (GAAGGACG GAGUACUAAUAdTdT) (18).…”

Section: Methodsmentioning

confidence: 99%

Cdc14A and Cdc14B Redundantly Regulate DNA Double-Strand Break Repair

Han

et al. 2015

Molecular and Cellular Biology

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bCdc14 is a phosphatase that controls mitotic exit and cytokinesis in budding yeast. In mammals, the two Cdc14 homologues, Cdc14A and Cdc14B, have been proposed to regulate DNA damage repair, whereas the mitotic exit and cytokinesis rely on another phosphatase, PP2A-B55␣. It is unclear if the two Cdc14s work redundantly in DNA repair and which repair pathways they participate in. More importantly, their target(s) in DNA repair remains elusive. Here we report that Cdc14B knockout (Cdc14B ؊/؊ ) mouse embryonic fibroblasts (MEFs) showed defects in repairing ionizing radiation (IR)-induced DNA doublestrand breaks (DSBs), which occurred only at late passages when Cdc14A levels were low. This repair defect could occur at early passages if Cdc14A levels were also compromised. These results indicate redundancy between Cdc14B and Cdc14A in DSB repair. Further, we found that Cdc14B deficiency impaired both homologous recombination (HR) and nonhomologous end joining (NHEJ), the two major DSB repair pathways. We also provide evidence that Cdh1 is a downstream target of Cdc14B in DSB repair.

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“…The HR defect in the absence of Brca1 is overcome by the removal of 53BP1 (Bunting et al 2010), suggesting that the balance between the two proteins is important for the regulation of HR. Depletion of RNF168, a E3 ubiquitin ligase required for 53BP1 recruitment, also suppressed the HR defect in Brca1-deficient cells (Munoz et al 2012). In addition to their functions in regulating DSB repair, Brca1 and 53BP1 contribute to the efficient phosphorylation of some ATM substrates and have been implicated in checkpoint activation (DiTullio et al 2002;Wang et al 2002;Fabbro et al 2004;Kitagawa et al 2004).…”

Section: Chromatin-mediated Dna-break Recognition By Atmmentioning

confidence: 99%

DNA Damage Sensing by the ATM and ATR Kinases

Maréchal

Zou

2013

Cold Spring Harbor Perspectives in Biology

1,167

952

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In eukaryotic cells, maintenance of genomic stability relies on the coordinated action of a network of cellular processes, including DNA replication, DNA repair, cell-cycle progression, and others. The DNA damage response (DDR) signaling pathway orchestrated by the ATM and ATR kinases is the central regulator of this network in response to DNA damage. Both ATM and ATR are activated by DNA damage and DNA replication stress, but their DNAdamage specificities are distinct and their functions are not redundant. Furthermore, ATM and ATR often work together to signal DNA damage and regulate downstream processes. Here, we will discuss the recent findings and current models of how ATM and ATR sense DNA damage, how they are activated by DNA damage, and how they function in concert to regulate the DDR.

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Ring Finger Nuclear Factor RNF168 Is Important for Defects in Homologous Recombination Caused by Loss of the Breast Cancer Susceptibility Factor BRCA1

Cited by 45 publications

References 57 publications

Regulation of Single-Strand Annealing and its Role in Genome Maintenance

Regulation of Single-Strand Annealing and its Role in Genome Maintenance

Cdc14A and Cdc14B Redundantly Regulate DNA Double-Strand Break Repair

DNA Damage Sensing by the ATM and ATR Kinases

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