Polyploidy Induced by X-rays in Chinese Hamster Cells in vitro

Science ◽  
1964 ◽  
Vol 145 (3631) ◽  
pp. 508-510 ◽  
Author(s):  
C. K. Yu ◽  
W. K. Sinclair

1972 ◽  
Vol 52 (3) ◽  
pp. 509 ◽  
Author(s):  
C. K. Yu ◽  
W. K. Sinclair


1970 ◽  
Vol 43 (3) ◽  
pp. 561 ◽  
Author(s):  
W. C. Dewey ◽  
S. C. Furman ◽  
H. H. Miller


1974 ◽  
Vol 10 (10) ◽  
pp. 691-693 ◽  
Author(s):  
Leo E. Gerweck ◽  
Edward L. Gillette ◽  
William C. Dewey


1972 ◽  
Vol 52 (1) ◽  
pp. 88 ◽  
Author(s):  
E. J. Hall ◽  
W. Gross ◽  
R. F. Dvorak ◽  
A. M. Kellerer ◽  
H. H. Rossi


Genetics ◽  
1969 ◽  
Vol 62 (2) ◽  
pp. 359-377
Author(s):  
E H Y Chu ◽  
Patricia Brimer ◽  
K B Jacobson ◽  
E Virginia Merriam


Genetics ◽  
1972 ◽  
Vol 72 (2) ◽  
pp. 239-252 ◽  
Author(s):  
F D Gillin ◽  
D J Roufa ◽  
A L Beaudet ◽  
C T Caskey

ABSTRACT Chinese hamster cells were treated with ethyl methanesulfonate or N-methyl-N'-nitro-N-nitrosoguanidine, and mutants resistant to 8-azaguanine were selected and characterized. Hypoxanthine-guanine phosphoribosyltransferase activity of sixteen mutants is extremely negative, making them suitable for reversion to HGPRTase+. Ten of the extremely negative mutants revert at a frequency higher than 10-7 suggesting their point mutational character. The remaining mutants have demonstrable HGPRTase activity and are not useful for reversion analysis. Five of these mutants have < 2% HGPRTase and are presumably also HGPRTase point mutants. The remaining 14 mutants utilize exogenous hypoxanthine for nucleic acid synthesis poorly, and possess 20-150% of wild-type HGPRTase activity in in vitro. Their mechanism of 8-azaguanine resistance is not yet defined.



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