Ku70 Is Required for DNA Repair but Not for T Cell Antigen Receptor Gene Recombination In Vivo

Ouyang, Honghai; Nussenzweig, Andre; Kurimasa, Akihiro; Soares, Vera da Costa; Li, Xiaoling; Cordon-Cardo, Carlos; Li, Wen-hui; Cheong, Nge; Nussenzweig, Michel; Iliakis, George; Chen, David J.; Li, Gloria C.

doi:10.1084/jem.186.6.921

Ku70 Is Required for DNA Repair but Not for T Cell Antigen Receptor Gene Recombination In Vivo

Journal Article · Mon Sep 15 00:00:00 EDT 1997 · Journal of Experimental Medicine

DOI:https://doi.org/10.1084/jem.186.6.921· OSTI ID:1625177

Ouyang, Honghai ^[1]; Nussenzweig, Andre ^[2]; Kurimasa, Akihiro ^[3]; Soares, Vera da Costa ^[2]; Li, Xiaoling ^[2]; Cordon-Cardo, Carlos ^[2]; Li, Wen-hui ^[4]; Cheong, Nge ^[4]; Nussenzweig, Michel ^[5]; Iliakis, George ^[4]; Chen, David J. ^[3]; Li, Gloria C. ^[2]

Memorial Sloan-Kettering Cancer Center, New York, NY (United States). Dept. of Medical Physics and Department of Radiation Oncology; DOE/OSTI
Memorial Sloan-Kettering Cancer Center, New York, NY (United States). Dept. of Medical Physics and Department of Radiation Oncology
Los Alamos National Lab. (LANL), Los Alamos, NM (United States)
Thomas Jefferson Univ., Philadelphia, PN (United States)
Rockefeller Univ., New York, NY (United States)

Ku is a complex of two proteins, Ku70 and Ku80, and functions as a heterodimer to bind DNA double-strand breaks (DSB) and activate DNA-dependent protein kinase. The role of the Ku70 subunit in DNA DSB repair, hypersensitivity to ionizing radiation, and V(D)J recombination was examined in mice that lack Ku70 (Ku70^–/–). Like Ku80^–/– mice, Ku70^–/– mice showed a profound deficiency in DNA DSB repair and were proportional dwarfs. Surprisingly, in contrast to Ku80^–/– mice in which both T and B lymphocyte development were arrested at an early stage, lack of Ku70 was compatible with T cell receptor gene recombination and the development of mature CD4+CD8^– and CD4^–CD8⁺ T cells. Our data shows, for the first time, that Ku70 plays an essential role in DNA DSB repair, but is not required for TCR V(D)J recombination. These results suggest that distinct but overlapping repair pathways may mediate DNA DSB repair and V(D)J recombination.

View Accepted Manuscript (DOE)

Research Organization:: Los Alamos National Laboratory (LANL), Los Alamos, NM (United States)

Sponsoring Organization:: USDOE Office of Science (SC), Biological and Environmental Research (BER). Biological Systems Science Division

Grant/Contract Number:: AC52-06NA25396

OSTI ID:: 1625177

Journal Information:: Journal of Experimental Medicine, Journal Name: Journal of Experimental Medicine Journal Issue: 6 Vol. 186; ISSN 0022-1007

Publisher:: Rockefeller University PressCopyright Statement

Country of Publication:: United States

Language:: English

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