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

Journal Article · Tue Jan 31 04:00:00 EST 1995 · Proceedings of the National Academy of Sciences of the United States of America

DOI:https://doi.org/10.1073/pnas.92.3.890· OSTI ID:50803

Doubnov, N V; Hall, K T; Wills, Z ^[1]; Lee, S E; He, D M; Benjamin, D M; Pulaski, C R; Hendrickson, E A ^[2]; Band, H ^[3]; Reeves, W ^[4]

---

1. Dana-Farber Cancer Institute, Boston, MA (United States)
2. Brown Univ., Providence, RI (United States)
3. Harvard Medical School, Boston, MA (United States)
4. Univ. of North Carolina, Chapel Hill, NC (United States)

Two ionizing radiation-sensitive (IR{sup 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{sup 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{sup s}, DNA end binding, and variable(diversity)joining [V(D)J] recombination signal and coding junction deficiencies of sci-3. Thus, the p86 Ku gene product is essential for DSB repair and V(D)J recombination.

• Sponsoring Organization: USDOE
• OSTI ID: 50803
• Journal Information: Proceedings of the National Academy of Sciences of the United States of America, Journal Name: Proceedings of the National Academy of Sciences of the United States of America Journal Issue: 3 Vol. 92; ISSN PNASA6; ISSN 0027-8424
• Country of Publication: United States
• Language: English

Related Subjects

56 BIOLOGY AND MEDICINE
APPLIED STUDIES
BIOCHEMISTRY
BIOLOGICAL RADIATION EFFECTS
DNA
IONIZING RADIATIONS
REPAIR
STRAND BREAKS