DNA-binding proteins articles within Nature

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  • Article |

    Comprehensive analyses of Cas9 proteins shed light on the evolution of the CRISPR–Cas9 system, and identify a pro-CRISPR accessory protein in bacteria that boosts CRISPR-mediated immunity by enhancing the DNA binding and cleavage activity of Cas9.

    • Shouyue Zhang
    • , Ao Sun
    •  & Jun-Jie Gogo Liu

  • Article
    | Open Access

    Cryo-electron microscopy structures of human RAD51 in complex with the nucleosome show that RAD51 can adopt two conformations—rings and filaments—and reveal how RAD51 binds to the nucleosome through its N-terminal lobe domain.

    • Takuro Shioi
    • , Suguru Hatazawa
    •  & Hitoshi Kurumizaka

  • Letter |

    Combining ancestral protein reconstruction with deep mutational scanning to characterize alternative histories in the sequence space around an ancient transcription factor reveals hundreds of alternative protein sequences that use diverse biochemical mechanisms to perform the derived function at least as well as the historical outcome.

    • Tyler N. Starr
    • , Lora K. Picton
    •  & Joseph W. Thornton

  • Letter |

    CRISPR/Cas9 DNA editing creates a double-stranded break in the target DNA, which can frequently generate random insertion or deletion of bases (indels); a new genome editing approach combining Cas9 with a cytidine deaminase is described here, which corrects point mutations more efficiently than canonical Cas9, while avoiding double-stranded breaks and indel formation.

    • Alexis C. Komor
    • , Yongjoo B. Kim
    •  & David R. Liu

  • Article |

    This study describes a new model of eukaryotic replication termination in which converging leading strands pass each other unhindered and the replicative DNA helicase is unloaded late, after all strands have been ligated.

    • James M. Dewar
    • , Magda Budzowska
    •  & Johannes C. Walter

  • Article |

    The crystal structure of the heterohexameric origin recognition complex (ORC), essential for coordinating DNA replication onset in eukaryotes, is resolved at 3.5 Å resolution.

    • Franziska Bleichert
    • , Michael R. Botchan
    •  & James M. Berger

  • Letter |

    Cell cycle checkpoints, such as the S-phase checkpoint, delay cell division to give the cell time to repair any damaged DNA. Here it is shown that the MLL gene — frequently disrupted in leukaemia — is part of the S-phase checkpoint. When DNA is damaged, MLL is phosphorylated by the ATR protein, causing MLL to accumulate on chromatin and methylate histone H3 on lysine 4. This delays DNA replication. MLL translocations, such as those that occur in leukaemia, disrupt this pathway and cause genomic instability.

    • Han Liu
    • , Shugaku Takeda
    •  & James J.-D. Hsieh

  • 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

  • Letter |

    TET1 is an enzyme that catalyses the conversion of 5-methylcytosine of DNA to 5-hydroxymethylcytosine, raising the possibility that it is involved in mediating DNA demethylation. These authors show that Tet1 is involved in mouse embryonic stem cell maintenance and specification of the inner cell mass. It is required to maintain both the expression of Nanog in embryonic stem cells and the Nanog promoter in a hypomethylated state, supporting a role for Tet1 in regulating DNA methylation.

    • Shinsuke Ito
    • , Ana C. D’Alessio
    •  & Yi Zhang

  • Letter |

    Most human gene promoters are embedded within CpG islands that lack DNA methylation and coincide with sites at which histone H3 lysine 4 is trimethylated (H3K4me3 sites). Here, a zinc-finger protein, Cfp1, is found to be associated with non-methylated CpG islands and H3K4me3 sites throughout the genome in the mouse brain. A primary function of non-methylated CpG islands might be to genetically determine the local chromatin modification state by interaction with Cfp1 and perhaps other CpG-binding proteins.

    • John P. Thomson
    • , Peter J. Skene
    •  & Adrian Bird

  • Letter |

    Most agents that generate breaks in DNA leave 'dirty ends' that cannot be joined immediately; instead, intervening steps are required to restore the integrity of nucleotides at the break. Here it is shown that the non-homologous end joining pathway requires a 5′-dRP/AP lyase activity to remove abasic sites at double-strand breaks. Surprisingly, this activity is catalysed by the Ku70 protein, which, together with its partner Ku86, had been thought only to recognize broken DNA ends and to recruit other factors that process ends.

    • Steven A. Roberts
    • , Natasha Strande
    •  & Dale A. Ramsden

  • Letter |

    Heterozygous mutations in the gene encoding CHD7, an ATP-dependent chromatin-remodelling protein, result in CHARGE syndrome — a disorder characterized by malformations of the craniofacial structures, peripheral nervous system, ears, eyes and heart. In humans and Xenopus, CHD7 is now shown to be essential for the formation of multipotent migratory neural crest and for activating the transcriptional circuitry of the neural crest; shedding light on the pathoembryology of CHARGE syndrome.

    • Ruchi Bajpai
    • , Denise A. Chen
    •  & Joanna Wysocka

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