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

Nikolai V. Boubnov, Kathryn T. Hall, Zachary Wills, Sang Eun Lee, Dong Ming He, Damien M. Benjamin, Cheryl R. Pulaski, Hamid Band, Westley Reeves, Eric A. Hendrickson, David T. Weaver

Research output: Contribution to journalArticlepeer-review

134 Scopus citations

Abstract

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. Cell fusions with xrs-6, another IR(s), DSB repair-deficient cell line, defined these sxi mutants in the XRCC5 group. sxi-3 cells have low expression 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 variable(diversity)joining [V(D)J] recombination signal and coding junction deficiencies of sxi-3. Thus, the p86 Ku gene product is essential for DSB repair and V(D)J recombination.

Original languageEnglish (US)
Pages (from-to)890-894
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume92
Issue number3
DOIs
StatePublished - Jan 31 1995

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