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

doi:10.1073/pnas.92.3.890

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

Biochemistry, Molecular Biology, and Biophysics (TMED)

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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 language	English (US)
Pages (from-to)	890-894
Number of pages	5
Journal	Proceedings of the National Academy of Sciences of the United States of America
Volume	92
Issue number	3
DOIs	https://doi.org/10.1073/pnas.92.3.890
State	Published - Jan 31 1995

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Boubnov, N. V., Hall, K. T., Wills, Z., Lee, S. E., He, D. M., Benjamin, D. M., Pulaski, C. R., Band, H., Reeves, W., Hendrickson, E. A., & Weaver, D. T. (1995). 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. Proceedings of the National Academy of Sciences of the United States of America, 92(3), 890-894. https://doi.org/10.1073/pnas.92.3.890

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. / Boubnov, Nikolai V.; Hall, Kathryn T.; Wills, Zachary et al.
In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 92, No. 3, 31.01.1995, p. 890-894.

Research output: Contribution to journal › Article › peer-review

Boubnov, NV, Hall, KT, Wills, Z, Lee, SE, He, DM, Benjamin, DM, Pulaski, CR, Band, H, Reeves, W, Hendrickson, EA & Weaver, DT 1995, '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', Proceedings of the National Academy of Sciences of the United States of America, vol. 92, no. 3, pp. 890-894. https://doi.org/10.1073/pnas.92.3.890

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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.",

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AU - Wills, Zachary

AU - Lee, Sang Eun

AU - He, Dong Ming

AU - Benjamin, Damien M.

AU - Pulaski, Cheryl R.

AU - Band, Hamid

AU - Reeves, Westley

AU - Hendrickson, Eric A.

AU - Weaver, David T.

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N2 - 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.

AB - 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.

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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

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