Checkpoint signalling articles within Nature

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  • Article
    | Open Access

    We uncover the mechanism underlying the restriction point phenomenon, suggest a role for cyclin-dependent kinase 4 and 6 activity in S and G2 phases, and explain the behaviour of cells following loss of mitogen signalling.

    • James A. Cornwell
    • , Adrijana Crncec
    •  & Steven D. Cappell

  • Letter |

    Mother cells transmit mitogen-induced CCND1 mRNA and DNA damage-induced p53 protein to newly born daughter cells, where synthesized cyclin D1 and the p53-regulated CDK inhibitor p21 directly compete to decide between proliferation and quiescence.

    • Hee Won Yang
    • , Mingyu Chung
    •  & Tobias Meyer

  • 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 |

    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.

    • Philip Zegerman
    •  & John F. X. Diffley

  • Letter |

    The ends of chromosomes, known as telomeres, look like ends generated by double-strand breaks, but if treated as such the DNA damage repair system would initiate a checkpoint response and cause telomere–telomere fusions. These authors show that telomeres lack two types of histone modification that are required for recruitment of Crb2b53BP1, without which the checkpoint cannot be activated even if other DNA damage response proteins are recruited to a Taz1-deficient telomere.

    • Tiago Carneiro
    • , Lyne Khair
    •  & Miguel Godinho Ferreira

  • Letter |

    Kinase regulatory pathways are used in eukaryotic DNA replication to facilitate coordination with other processes during cell division cycles and response to environmental cues. The Dbf4–Cdc7 kinase (DDK) is one of at least two cell-cycle-regulated protein kinase systems essential for initiation of DNA replication. DDK is now shown to relieve the inhibitory activity of the amino-terminal domain of the replicative helicase Mcm4, thus promoting S phase.

    • Yi-Jun Sheu
    •  & Bruce Stillman

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