Telomeres articles within Nature Cell Biology

Featured

  • News & Views |

    Cellular senescence induced by DNA replication and telomere attrition contributes to organ dysfunction, inflammation and impaired immunity. A study reveals that antigen-presenting cells provide telomeric DNA to CD4+ T cells in synaptic contact, which enables the suspension of senescence, T cell expansion and long-lived immunity.

    • Anna Carey
    • , Laura Niedernhofer
    •  & Christina Camell

  • Review Article |

    Rossiello et al. review the contributions of telomere shortening and/or dysfunction to ageing and a broad spectrum of age-associated human diseases.

    • Francesca Rossiello
    • , Diana Jurk
    •  & Fabrizio d’Adda di Fagagna

  • Article |

    Both telomerase activity and NF-κB-driven inflammation occur in tumours, and NF-κB is known to upregulate telomerase levels. Tergaonkar and colleagues now find evidence for a reciprocal direct regulation of NF-κB-dependent gene transcription by telomerase, through an interaction between telomerase and the NF-κB p65 subunit.

    • Arkasubhra Ghosh
    • , Gaye Saginc
    •  & Vinay Tergaonkar

  • News & Views |

    Cellular senescence is a stable proliferation arrest induced by triggers such as short telomeres, activated oncogenes and genotoxic stress. Two studies show that cellular senescence induced by genotoxic stress depends on chronic DNA-damage signalling from irreparable damage to telomeres. Hence, dysfunctional or damaged telomeres are the initiators of multiple modes of senescence.

    • John van Tuyn
    •  & Peter D. Adams

  • Article |

    D’Adda di Fagagna and colleagues observe that, after genotoxic treatment of cells and mice, unrepaired DNA-damage foci and DNA-damage signalling persist at telomeres. They show that introducing the telomeric protein TRF2 near a double-strand break elsewhere on the chromosomes prevents repair. Unrepaired foci are also observed at telomeres of ageing animals, suggesting a role for TRF2 in senescence establishment.

    • Marzia Fumagalli
    • , Francesca Rossiello
    •  & Fabrizio d’Adda di Fagagna

  • Letter |

    The E3 ligase RNF8 is recruited to double-strand breaks in DNA to promote repair. Jacobs and colleagues discovered that RNF8 also goes to unprotected telomeres, where it mediates non-homologous end-joining of chromosome ends and contributes to telomere-induced genomic instability.

    • Marieke H. Peuscher
    •  & Jacqueline J. L. Jacobs

  • News & Views |

    Three recent studies reveal unexpected functions of Rap1, a member of the shelterin complex that protects chromosome ends from the activity of DNA repair pathways. Rap1 not only protects telomeres from sister chromatid exchange, but also functions in genome-wide transcriptional regulation and NF-κB-dependent signalling, revealing new perspectives for the telomere field.

    • Laure Crabbe
    •  & Jan Karlseder

Browse broader subjects

Browse Telomeres across other nature.com journals