DNA repair is crucial for maintaining hematopoietic stem cell function

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Richard Cornall and collaborators recently developed a mouse model of Ligase IV syndrome with growth retardation and immunodeficiency due to a defect in nonhomologous end-joining (NHEJ) of DNA double-strand breaks. They demonstrated age-dependent loss of hematopoietic stem cell function in these mice. Simultaneously, Irving Weissman and colleagues demonstrated a similar phenomenon in Ku80-/- mice defective in NHEJ and telomere maintenance, XpdTTD mice defective in nucleotide excision repair, and late generation mTr-/- missing telomerase activity. These studies strongly support the hypothesis that genomic stress causes aging by limiting the ability of stem cells to indefinitely maintain tissue homeostasis.

Original languageEnglish (US)
Pages (from-to)523-529
Number of pages7
JournalDNA Repair
Issue number3
StatePublished - Mar 1 2008
Externally publishedYes

Bibliographical note

Funding Information:
L.J.N. is supported by The Ellison Medical Foundation (AG-NS-0303-05), the NCI (CA111525 and CA10370) and the University of Pittsburgh Cancer Institute.


  • Aging
  • Endogenous damage
  • Oxidative stress
  • Progeria


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