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Ataxia-Telangiectasia-like Chinese Hamster V79 Cell Mutants with Radioresistant DNA Synthesis, Chromosomal Instability, and Normal DNA Strand Break Repair¹

Magorzata Z. Zdzienicka², Nicolaas G. J. Jaspers, Govert P. van der Schans, Adayapalam T. Natarajan and Johannes W. I. M. Simons

Department of Radiation Genetics and Chemical Mutagenesis, State University of Leiden, Wassenaarseweg 72, 2333 AL Leiden [M. Z. Z., A. T. N., J. W. I. M. S.]; Department of Cell Biology and Genetics, Erasmus University, P. O. Box 1738, 3000 DR Rotterdam [N. G. J. J.]; TNO Medical Biological Laboratory, Rijswijk [G. P. v. d. S.]; and J. A. Cohen Institute, Interuniversity Research Institute for Radiopathology and Radiation Protection, [A. T. N.] The Netherlands

We have isolated three radiosensitive mutants (V-C4, V-E5, and V-G8) of the Chinese hamster V79 cell line which also show increased sensitivities to killing by bleomycin (2-5-fold) and ethyl methanesulfonate (2-fold). Genetic complementation analysis indicates that all three mutants belong to one complementation group. The mutants show a radioresistant DNA synthesis following X-ray irradiation when compared to wild-type V79 cells. Both the level and the rate of repair of DNA single- and double-strand breaks measured by DNA elution were similar to those observed in wild-type V79 cells. The level of spontaneously occurring chromosome aberrations in two of these mutants differs severalfold from the level observed in wild-type V-79 cells and in V-G8, to 2- and 6-fold increase in V-E5 and V-C4, respectively. X-irradiation of the mutants resulted in consistently 3-4-fold higher levels of chromatid gaps, breaks, and exchanges than observed in wild-type V79 cells. In addition, G₁ irradiation of the mutant cells yielded both chromsome and chromatid types of aberrations. The level and pattern of chromosomal aberrations induced by X-rays in V-C4, V-E5, and V-G8 are similar to those observed in ataxia-telangiectasia cells.

These results indicate that our mutants represent the first rodent cell mutants which show phenotypic characteristics strongly resembling those in cells from ataxia-telangiectasia patients.

¹ This work was supported by the Foundation of Basic Medical Research (MEDIGON) Grant 13-23-91, the Commission of the European Communities, Contracts ENV-534-NL and BIO-E-407-NL, and the J. A. Cohen Institute.

² To whom requests for reprints should be addressed.

Received 9/21/88. Revised 11/22/88. Accepted 12/14/88.

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