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    EMBO Rep. 2004 May;5(5):503-9. Epub 2004 Apr 23.

    Shorter telomeres, accelerated ageing and increased lymphoma in DNA-PKcs-deficient mice.

    Espejel S, Martín M, Klatt P, Martín-Caballero J, Flores JM, Blasco MA.

    Source

    Molecular Oncology Program, Spanish National Cancer Centre (CNIO), Melchor Fernández Almagro 3, E-28029, Madrid, Spain.

    Abstract

    Non-homologous end joining (NHEJ) is the principal repair mechanism used by mammalian cells to cope with double-strand breaks (DSBs) that continually occur in the genome. One of the key components of the mammalian NHEJ machinery is the DNA-PK complex, formed by the Ku86/70 heterodimer and the DNA-PK catalytic subunit (DNA-PKcs). Here, we report on the detailed life-long follow-up of DNA-PKcs-defective mice. Apart from defining a role of DNA-PKcs in telomere length maintenance in the context of the ageing organism, we observed that DNA-PKcs-defective mice had a shorter life span and showed an earlier onset of ageing-related pathologies than the corresponding wild-type littermates. In addition, DNA-PKcs ablation was associated with a markedly higher incidence of T lymphomas and infections. In conclusion, these data link the dual role of DNA-PKcs in DNA repair and telomere length maintenance to organismal ageing and cancer.

    PMID:
    15105825
    [PubMed - indexed for MEDLINE]
    PMCID:
    PMC1299048
    Free PMC Article

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