Homologous recombination articles within Nature

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  • Article
    | Open Access

    Observations of rapid repair of double-stranded DNA breaks in sister choromosomes in Escherichia coli are consistent with a reduced-dimensionality-search model of RecA-mediated repair.

    • Jakub Wiktor
    • , Arvid H. Gynnå
    •  & Johan Elf

  • Article |

    A tandem BRCT-domain-associated ubiquitin-dependent recruitment motif in BARD1 recruits BRCA1 to DNA double-strand breaks (DSBs) to promote homologous recombination and antagonize the 53BP1 DSB repair pathway that mediates non-homologous end joining.

    • Jordan R. Becker
    • , Gillian Clifford
    •  & J. Ross Chapman

  • Article |

    DYNLL1 antagonizes end resection of DNA double-strand breaks, thereby inhibiting homologous repair, and the loss of DYNLL1 correlates with poor progression-free survival of patients with BRCA1-mutant ovarian cancer.

    • Yizhou Joseph He
    • , Khyati Meghani
    •  & Dipanjan Chowdhury

  • Article |

    The tumour suppressor complex BRCA1–BARD1, which facilitates the generation of a single-stranded DNA template during homologous recombination, also binds to the recombinase RAD51 and enhances its function.

    • Weixing Zhao
    • , Justin B. Steinfeld
    •  & Patrick Sung

  • Letter |

    A mechanism for the repression of homologous recombination in G1, the stage of the cell cycle preceding replication, is determined; the critical aspects are the interaction between BRCA1 and PALB2–BRCA2, and suppression of DNA-end resection.

    • Alexandre Orthwein
    • , Sylvie M. Noordermeer
    •  & Daniel Durocher

  • Letter |

    Loss of REV7 is shown to regulate end resection of double-stranded DNA breaks in BRCA1-deficient cells, leading to PARP inhibitor resistance and restoration of homologous recombination; REV7 dictates pathway choice in BRCA1-deficient cells and during immunoglobulin class switching.

    • Guotai Xu
    • , J. Ross Chapman
    •  & Sven Rottenberg

  • Letter |

    In studies in mammalian cells, polymerase theta (Polθ, also known as POLQ) is identified as the polymerase responsible for non-homologous end joining DNA repair; this DNA repair pathway acts in many tumours when homologous recombination is inactivated and the identification of the polymerase responsible may aid the development of new therapeutic approaches.

    • Raphael Ceccaldi
    • , Jessica C. Liu
    •  & Alan D. D’Andrea

  • Letter |

    Meiotic recombination is initiated by a fairly uniform distribution of hundreds of DNA double-strand breaks catalysed by the Spo11 protein; here, Tel1 (orthologue of human ATM) is shown to be required for the localized inhibition that prevents double-strand breaks from forming close to one another.

    • Valerie Garcia
    • , Stephen Gray
    •  & Matthew J. Neale

  • Letter |

    The MRX complex, required for double-strand break (DSB) repair by homologous recombination, has 3′ to 5′ exonuclease activity, but homologous recombination at a DSB uses a 3′-tailed molecule, which requires resection of the 5′ strand; here it is shown that in yeast, Sae2 nuclease promotes MRX to make an initial endonucleolytic cut on the 5′ strand that may allow MRX to digest the 5′ strand back to the end in a 3′ to 5′ fashion.

    • Elda Cannavo
    •  & Petr Cejka

  • Letter |

    A dual-function helicase–nuclease, typified by RecBCD in Escherichia coli, acts on free DNA ends during bacterial double-stranded break repair until it reaches a χ sequence at which it pauses before continuing with modified enzymatic properties; here several crystal structures of the related AddAB enzyme from Bacillus subtilis bound to χ-containing DNA are presented, offering insight into χ recognition and its effect on DNA translocation.

    • Wojciech W. Krajewski
    • , Xin Fu
    •  & Dale B. Wigley

  • Letter |

    A new mechanism of chromosomal rearrangement is identified through the observation that broken or collapsed DNA replication forks restarted by homologous recombination have a high propensity for U-turns at short inverted repeats; the error-prone nature of this mechanism is suggested to contribute to gross chromosomal rearrangements and copy-number variations present in cancer and other genomic disorders.

    • Ken’Ichi Mizuno
    • , Izumi Miyabe
    •  & Johanne M. Murray

  • Letter |

    When double-strand breaks occur in DNA, the broken ends must undergo processing to prepare them for repair. Here, and in an accompanying study, this processing reaction has now been replicated in vitro using yeast proteins. Processing minimally requires the activities of a helicase, a nuclease and a single-strand-binding protein, although the reaction is enhanced by the addition of three factors that help to target the core complex and stimulate the unwinding activity.

    • Petr Cejka
    • , Elda Cannavo
    •  & Stephen C. Kowalczykowski

  • Article |

    The two hereditary breast cancer susceptibility genes, BRCA1 and BRCA2, have roles in responding to DNA damage. When they are mutated or absent, genomic instability, a contributory factor to cancer development, results. Studies of BRCA2 have been hampered by its large size, which makes purification of the full-length protein challenging. These authors report the first in vitro characterization of full-length BRCA2 and delineate the different ways by which BRCA2 facilitates RAD51-mediated homologous recombination.

    • Ryan B. Jensen
    • , Aura Carreira
    •  & Stephen C. Kowalczykowski

  • Letter |

    The rat is a animal model widely used for studying human physiology and disease, but functional genomics and genetic research have been stifled by the limited availability of gene targeting tools. These authors have established gene targeting by homologous recombination in rat embryonic stem cells, and have generated p53 gene knockout rats for the first time.

    • Chang Tong
    • , Ping Li
    •  & Qi-Long Ying

  • Letter |

    In meiotic cells paired homologues are joined by a set of crossovers known as a double Holliday junction (DHJ). Whether DHJs form during mitotic recombination has been unclear, as mitotic cells possess alternative repair pathways that would not require DHJ formation. Here it is demonstrated that mitotic and meiotic cells form similar DHJs, but that the levels in mitotic cells are approximately 10–fold lower, and show a preference for joints between sister chromatids rather than homologues. Consequently, in mitotic cells non–crossover outcomes are favoured.

    • Malgorzata Bzymek
    • , Nathaniel H. Thayer
    •  & Neil Hunter

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