Inverse relationship between galactokinase activity and 2-deoxygalactose resistance in Chinese hamster ovary cells

Springer Science and Business Media LLC - Tập 4 - Trang 699-713 - 1978
Carolyn D. Whitfield1, Bruce Buchsbaum2, Richard Bostedor1, Ernest H. Y. Chu2
1Department of Biological Chemistry, University of Michigan, Ann Arbor
2Department of Human Genetics, University of Michigan, Ann Arbor

Tóm tắt

Galactokinase activity is reduced in 12 independent clones of Chinese hamster ovary cells resistant to 2-deoxygalactose. The frequency of resistant colonies is increased with chemical mutagens. The resistant phenotype is stable in the absence of selection. There is an inverse correlation between the levels of galactokinase activity and the cloning efficiency in deoxygalactose. Cells with high resistance have 1%or less of the enzyme activity observed in the parental cells; while cells with low resistance have 10–30% galactokinase activity. Studies with tetraploid hybrid cells reveal that resistance to deoxygalactose is a recessive trait and that cells with high resistance do not complement those with low resistance. In cell lines with low resistance, the K m for galactose, K i for deoxygalactose, K m for ATP, and thermolability were not significantly altered compared to sensitive parental cells. Although the possibility of mutation at the structural gene locus has not been ruled out, the reduced enzyme activity may also be due to mutation at a regulatory site which affects the number of galactokinase molecules per cell.

Tài liệu tham khảo

Alper, M. D., and Ames, B. N. (1975).J. Bacteriol. 121:259–266. Nagelkerke, F., and Postma, P. W. (1978).J. Bacteriol. 133:607–613. Thirion, J.-P., Banville, D., and Noel, H. (1976).Genetics 83:137–147. Whitfield, C. D., and Chu, E. H. Y. (1976).Experta Med. Int. Congr. Ser. 397:55. Eagle, H. (1959).Science 130:432–437. McBurney, M. W.,and Whitmore, G. F. (1976).Cell 2:173–182. Taylor, R. T., and Hanna, M. L. (1977).Arch. Biochem. Biophys. 181:331–344. Chu, E. H. Y., and Powell, S. S. (1976). InAdv. Hum. Genet, Vol. 7 (ed. by Harris, H., and Hirschhorn, K.) (Plenum Press, New York), pp. 189–258. Davidson, R. L., O'Malley, K. A., and Wheeler, T. B. (1976)Somat. Cell Genet. 2:271–280. Stutts, P., and Brockman, R. W. (1963).Biochem. Pharmacol. 12:97–104. Sharp, J. D., Capecchi, N. E., and Capecchi, M. R. (1973).Proc. Natl. Acad. Sci. U.S.A. 70:3145–3149. Farrell, S. A., and Worton, R. G. (1977).Somat. Cell Genet. 3:539–551. Littlefield, J. W. (1964).Science 145:709. Chu, E. H. Y., Brimer, P., Jacobson, K. B., and Merriam, E. V. (1969).Genetics 62:359–377. Lowry, O. H., Rosebrough, N. J., Farr, A. L., and Randall, R. J. (1951).J. Biol. Chem. 193:265–275. Sherman, J. R., and Adler, J. (1963).J. Biol. Chem. 238:873–878. Beutler, E. (1975).Red Cell Metabolish, 2nd ed. (Grune & Stratton, New York), pp. 97–102. Mayes, J. S. and Hansen, R. G. (1966). InMethods in Enzymology, Vol. 9 (ed. by Wood, W. A.) (Academic Press, New York), pp. 708–713. Segel, I. H. (1975).Enzyme Kinetics (J. Wiley, New York), pp. 108–109. Worton, R. G., Ho, C. C., and Duff, C. (1977).Somat. Cell Genet. 3:27–45. Siminovitch, L. (1976).Cell 7:1–11. Chasin, L. A. (1973).J. Cell Physiol. 82:299–308. Elsevier, S. M., Kucherlapati, R. S., Nichols, E. A., Creagan, R. P., Giles, R. E., Ruddle, F. H., Willecke, K., and McDougall, J. K. (1974).Nature 251:633–635. Orkwiszewski, K. G., Tedesco, T. A., Mellman, W. J., and Croce, C. M. (1976).Somat. Cell Genet. 2:21–26. Kozak, C. A., and Ruddle, F. H. (1977).Somat. Cell Genet. 3:121–133. Smith, D. F., and Keppler, D. O. R. (1977).Eur. J. Biochem. 73:83–92. Starling, J. J., and Keppler, D. O. R. (1977).Eur. J. Biochem. 80:373–379. Wilson, D. B., and Hogness, D. S. (1966). InMethods in Enzymology, Vol. 8 (eds.) Neufeld, E. F., and Ginsburg, V. (Academic Press, New York), pp. 229–240.