Abstract
Wild-type cells and thymidine kinase-deficient clones from two mouse lymphoma cell lines, P388 and L5178Y, were compared for sensitivity to killing by the mutagens, ultraviolet irradiation (UV), ethyl methane sulfonate (EMS), and N-methyl-N′-nitro-N-nitrosoguanidine (MNNG). Two out of three thymidine kinase-deficient P388 clones showed significantly enhanced sensitivity to killing by all three mutagens. This increased sensitivity to killing was also reflected in increased mutagenesis by the three mutagens. In the L5178Y cell line, wild-type cells showed little difference to two thymidine kinase-deficient clones in terms of mutagen sensitivity. This indicates that thymidine kinase may be significant for DNA repair processes in P388 but not in L5178Y cells. Unscheduled DNA synthesis (UDS) experiments were carried out on P388 and L5178Y wild-type cells and wild-type Friend leukemia cells (which are mutagen-sensitive when deficient in thymidine kinase). The UDS experiments showed the L5178Y cells were low in excision repair abilities relative to the P388 cells and the Friend cell clone. This indicates that the increased mutagen sensitivity in thymidine kinase-deficient P388 and clone 707 Friend cells may be due to thymidine kinase playing an indirect role in DNA excision repair, a process which is of little significance in the L5178Y cell line.
Similar content being viewed by others
Literature cited
McKenna, P.G. (1980).Heredity 45:155.
McKenna, P.G., and Hickey, I. (1981).Cell Biol. Int. Rep. 5:555–561.
McKenna, P.G., and Yasseen, A.A. (1982).Genet. Res. 40:207–212.
Yasseen, A.A., and McKenna, P.G. (1983).Heredity 50:207–208.
McKenna, P.G., and Yasseen, A.A. (1984).Leukemia Res. (in press).
Scher, W., Holland, J.G., and Friend, C. (1971).Blood 37:428–437.
Fox, M., and Gilbert, C.W. (1966).Int. J. Radiat. Biol. 11:339–347.
McKenna, P.G., and Hickey, I. (1981).Mutat. Res. 80:187–199.
Fischer, G.A. (1958).Ann. N. Y. Acad. Sci. 76:673–680.
Breitman, T.R. (1963).Biochim. Biophys. Acta 67:153–155.
Cleaver, J.E., and Thomas, G.H. (1981). InDNA Repair—A Laboratory Manual of Research Procedures, Vol. 1B, (eds.) Friedberg, E.C., and Hanawalt, P.C. (Marcel Dekker, New York), pp. 277–287.
Lehmann, A.R. (1972).Eur. J. Biochem. 31:438–445.
Sato, K., and Setlow, R.B. (1981).Mutat. Res. 84:443–455.
Ayad, S.R., and Fox, B.W. (1969).Mutat. Res. 8:639–645.
Moore, E.C., and Hulbert, R.B. (1966).J. Biol. Chem. 241:2540–2549.
Brown, N.C., and Reichard, P. (1969).J. Mol. Biol. 46:39–55.
Cleaver, J.E. (1978).Biochim. Biophys. Acta 516:489–516.
Bradley, M.D., and Sharkey, N. (1978).Nature 274:607–608.
Peterson, A.R., Landolph, J.R., Peterson, H., and Heidelberger, C. (1978).Nature 276:508–510.
Meuth, M. (1981).Somat. Cell Genet. 7:89–102.
Yasseen, A.A., and McKenna, P.G. (1983).Experientia 39:532–534.
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
McKenna, P.G., Yasseen, A.A. & McKelvey, V.J. Evidence for indirect involvement of thymidine kinase in excision repair processes in mouse cell lines. Somat Cell Mol Genet 11, 239–246 (1985). https://doi.org/10.1007/BF01534680
Received:
Revised:
Issue Date:
DOI: https://doi.org/10.1007/BF01534680