Double strand break rejoining by the Ku-dependent mechanism of non-homologous end-joining

C R Acad Sci III. 1999 Feb-Mar;322(2-3):109-12. doi: 10.1016/s0764-4469(99)80031-6.

Abstract

The DNA-dependent protein kinase functions in the repair of DNA double strand breaks (DSBs) and in V(D)J recombination. To gain insight into the function of DNA-PK in this process we have carried out a mutation analysis of Ku80 and DNA-PKcs. Mutations at multiple sites within the N-terminal two thirds of Ku80 result in loss of Ku70/80 interaction, loss of DNA end-binding activity and inability to complement Ku80 defective cell lines. In contrast, mutations in the carboxy terminal region of the protein do not impair DNA end-binding activity but decrease the ability of Ku to activate DNA-PK. To gain insight into important functional domains within DNA-PKcs, we have analysed defective mutants, including the mouse scid cell line, and the rodent mutants, irs-20 and V-3. Mutational changes in the carboxy terminal region have been identified in all cases. Our results strongly suggest that the C-terminus of DNA-PKcs is required for kinase activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Cricetinae
  • DNA Repair*
  • DNA-Activated Protein Kinase
  • DNA-Binding Proteins / metabolism*
  • Mice
  • Mutation
  • Protein Serine-Threonine Kinases / metabolism
  • Recombination, Genetic*
  • Sequence Homology, Nucleic Acid

Substances

  • DNA-Binding Proteins
  • DNA-Activated Protein Kinase
  • Protein Serine-Threonine Kinases