scholarly journals Promotion of Homologous Recombination and Genomic Stability by RAD51AP1 via RAD51 Recombinase Enhancement

2007 ◽  
Vol 28 (3) ◽  
pp. 482-490 ◽  
Author(s):  
Claudia Wiese ◽  
Eloïse Dray ◽  
Torsten Groesser ◽  
Joseph San Filippo ◽  
Idina Shi ◽  
...  
Keyword(s):  
Homologous Recombination ◽  
Genomic Stability

scholarly journals Author response: MicroRNAs down-regulate homologous recombination in the G1 phase of cycling cells to maintain genomic stability

2014 ◽  
Author(s):  
Young Eun Choi ◽  
Yunfeng Pan ◽  
Eunmi Park ◽  
Panagiotis Konstantinopoulos ◽  
Subhajyoti De ◽  
...  
Keyword(s):  
Homologous Recombination ◽  
Genomic Stability ◽  
Author Response ◽  
G1 Phase

scholarly journals RTEL1 Maintains Genomic Stability by Suppressing Homologous Recombination

Cell ◽  
2008 ◽  
Vol 135 (2) ◽  
pp. 261-271 ◽  
Author(s):  
Louise J. Barber ◽  
Jillian L. Youds ◽  
Jordan D. Ward ◽  
Michael J. McIlwraith ◽  
Nigel J. O'Neil ◽  
...  
Keyword(s):  
Homologous Recombination ◽  
Genomic Stability

scholarly journals A YY1–INO80 complex regulates genomic stability through homologous recombination–based repair

2007 ◽  
Vol 14 (12) ◽  
pp. 1165-1172 ◽  
Author(s):  
Su Wu ◽  
Yujiang Shi ◽  
Peter Mulligan ◽  
Frédérique Gay ◽  
Joseph Landry ◽  
...  
Keyword(s):  
Homologous Recombination ◽  
Genomic Stability

scholarly journals CtIP-mediated resection is essential for viability and can operate independently of BRCA1

2014 ◽  
Vol 211 (6) ◽  
pp. 1027-1036 ◽  
Author(s):  
Federica Polato ◽  
Elsa Callen ◽  
Nancy Wong ◽  
Robert Faryabi ◽  
Samuel Bunting ◽  
...  
Keyword(s):  
Homologous Recombination ◽  
Mouse Models ◽  
Genomic Stability ◽  
Homology Search ◽  
Genome Integrity ◽  
Parp Inhibition ◽  
Dna End Resection ◽  
End Resection ◽  
Dna Ends ◽  
Deficient Mice

Homologous recombination (HR) is initiated by DNA end resection, a process in which stretches of single-strand DNA (ssDNA) are generated and used for homology search. Factors implicated in resection include nucleases MRE11, EXO1, and DNA2, which process DNA ends into 3′ ssDNA overhangs; helicases such as BLM, which unwind DNA; and other proteins such as BRCA1 and CtIP whose functions remain unclear. CDK-mediated phosphorylation of CtIP on T847 is required to promote resection, whereas CDK-dependent phosphorylation of CtIP-S327 is required for interaction with BRCA1. Here, we provide evidence that CtIP functions independently of BRCA1 in promoting DSB end resection. First, using mouse models expressing S327A or T847A mutant CtIP as a sole species, and B cells deficient in CtIP, we show that loss of the CtIP-BRCA1 interaction does not detectably affect resection, maintenance of genomic stability or viability, whereas T847 is essential for these functions. Second, although loss of 53BP1 rescues the embryonic lethality and HR defects in BRCA1-deficient mice, it does not restore viability or genome integrity in CtIP−/− mice. Third, the increased resection afforded by loss of 53BP1 and the rescue of BRCA1-deficiency depend on CtIP but not EXO1. Finally, the sensitivity of BRCA1-deficient cells to poly ADP ribose polymerase (PARP) inhibition is partially rescued by the phospho-mimicking mutant CtIP (CtIP-T847E). Thus, in contrast to BRCA1, CtIP has indispensable roles in promoting resection and embryonic development.

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