COMPLEMENTATION OF THE IONIZING-RADIATION SENSITIVITY, DNA END BINDING, AND V(D)J RECOMBINATION DEFECTS OF DOUBLE-STRAND BREAK REPAIR MUTANTS BY THE P86 KU AUTOANTIGEN

Two ionizing radiation-sensitive (IR(s)) and DNA double-strand break ( DSB) mutants, sxi-3 and sxi-2, were shown to be severely deficient in a DNA end binding activity, similar to a previously described activity of the Ku autoantigen, correlating with the xrs (XRCC5) mutations. Ce ll fusions with xrs-6, another IR(s), DSB repair-deficient cell line, defined these sri mutants in the XRCC5 group. sxi-3 cells have low exp ression levels of the p86Ku mRNA, Introduction of the Ku p86 gene, but not the p70 Ku gene, complemented the IR(s), DNA end binding, and var iable(diversity)joining [V(D)J] recombination signal and coding juncti on deficiencies of sxi-3. Thus, the p86 Ku gene product is essential f or DSB repair and V(D)J recombination.