DNA damage checkpoints articles within Nature

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  • Article |

    KAT5 tyrosine phosphorylation, mediated by the tyrosine kinase c-Abl, increases after DNA damage, promoting KAT5 binding to histone H3K9me3, which triggers KAT5-mediated acetylation of the ATM kinase; this promotes the activation of the DNA damage checkpoint and cell survival.

    • Abderrahmane Kaidi
    •  & Stephen P. Jackson

  • 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 |

    DNA damage or replication stress induces the activation of checkpoint kinases, pausing the cell cycle so that DNA repair can take place; checkpoint activation must be regulated to prevent the cell-cycle arrest from persisting after damage is repaired, and now the Slx4–Rtt107 complex is shown to regulate checkpoint kinase activity by directly monitoring DNA-damage signalling.

    • Patrice Y. Ohouo
    • , Francisco M. Bastos de Oliveira
    •  & Marcus B. Smolka

  • Letter |

    Two classes of enzyme — cyclin-dependent kinases (CDK) and Dbf4-dependent kinase (DDK) — facilitate the initiation of DNA replication in eukaryotes. It is now shown that, when DNA damage is sensed, another kinase, Rad53, halts the firing of late replication origins by inhibiting both the CDK and the DDK pathways. Rad53 acts on DDK directly by inhibiting Dbf4, whereas the CDK pathway is blocked by Rad53-mediated phosphorylation of the downstream CDK substrate Sld3.

    • Jaime Lopez-Mosqueda
    • , Nancy L. Maas
    •  & David P. Toczyski

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