Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 97, Issue 6, Pages 2668-2673Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.97.6.2668
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- NINDS NIH HHS [R01NS36949] Funding Source: Medline
- PHS HHS [A.I.35714, A.I.01428] Funding Source: Medline
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Mammalian nonhomologous DNA end joining employs Ku70, Ku80. DNA-dependent protein kinase catalytic subunit (DNA-PKcs), XRCC4 and DNA ligase IV (Lig4). Herein, we show that Ku70 and Ku80 deficiency but not DNA-PKcs deficiency results in dramatically increased death of developing embryonic neurons in mice. The Ku-deficient phenotype is qualitatively similar to, but less severe than, that associated with XRCC4 and Lig4 deficiency. The lack of a neuronal death phenotype in DNA-PKcs-deficient embryos and the milder phenotype of Ku-deficient versus XRCC4- or Lig4-deficient embryos correlate with relative leakiness of residual end joining in these mutant backgrounds as assayed by a V(D)J recombination end joining assay. We conclude that normal development of the nervous system depends on the four evolutionarily conserved nonhomologous DNA end joining factors.
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