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- Title
Shorter telomeres, accelerated ageing and increased lymphoma in DNA-PKcs-deficient mice.
- Authors
Espejel, Silvia; Martín, Marta; Klatt, Peter; Martín-Caballero, Juan; Flores, Juana M; Blasco, María A
- 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.
- Publication
EMBO reports, 2004, Vol 5, Issue 5, p503
- ISSN
1469-221X
- Publication type
Journal Article
- DOI
10.1038/sj.embor.7400127