Mutagenesis to aminopterin resistance in cultured hamster cells

摘要: Abstract Spontaneous hamster cell mutants resistant to aminopterin have been shown previously contain an elevated folate reductase activity, not corrected upon somatic hybridization with low enzyme parent lines. In attempt isolate other types of we employed the chemical mutagens, ethylmethane sulfonate and nitrosoguanidine. Mutants resistance were produced at increased frequency, but highly clones could be directly these agents. Highly lines obtained by a second exposure mutagens. Unexpectedly, induced contained no more than wild-type cells. Mechanisms considered possible from work in systems excluded here decreased sensitivity inhibition drug, thymidylate synthetase drug uptake. Drug catabolism or metabolism derivatives within may altered mutants. These results underscore importance defining biochemical alterations mutants, suggest that mutagens particularly useful production novel animal systems.