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Department of Radiological Health Sciences, Colorado State University, Fort Collins, Colorado 80523-1673 [R. O., J. S. B.]; Department of Radiation Oncology-Biology Division, University of Texas Medical Branch, Galveston, Texas 77555-0656 [R. O., K. S., Y. Y., R. L. U.]; and National Radiological Protection Board, Chilton, Didcot, Oxon OX11 0RQ, United Kingdom [A. S., R. C.]
We have studied the efficiency of DNA double strand break (DSB)
rejoining in primary cells from mouse strains that show large
differences in in vivo radiosensitivity and tumor
susceptibility. Cells from radiosensitive, cancer-prone BALB/c mice
showed inefficient end joining of 
ray-induced DSBs as compared with
cells from all of the other commonly used strains and F1
hybrids of C57BL/6 and BALB/c mice. The BALB/c repair phenotype was
accompanied by a significantly reduced expression level of DNA-PKcs
protein as well as a lowered DNA-PK activity level as compared with the
other strains. In conjunction with published reports, these data
suggest that natural genetic variation in nonhomologous end joining
processes may have a significant impact on the in vivo
radiation response of mice.
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