AbstractTo examine the dependence on exposure rate of killing and mutagenesis by γ‐rays, two lines of Chinese hamster cells were studied. V79 cells were used to induce 6‐thioguanine resistance (6‐TGr) due to a mutation of the constitutive gene hypoxanthine‐guanine phosphoribosyl transferase (hgprt). Mutation of the bacterial geneguanine phosphoribosyl transferase (gpt) was studied in a line of mutated CHO cells,hgprt—which carried a single copy of gpt—by scoring cells that became 6‐TGr. The purpose of the study was to determine if the induction of either the mutant phenotypes or genotypes depended on dose rate, i.e., presumably were influenced by repair. To simulate a cell‐renewal population of cells in vivo, low enough dose rates of γ‐rays were used which permitted essentially continuous growth for 50–100 doublings in cell number. Considerable repair of mutagenesis as well as lethality was evident. Compared to exposures at high‐dose‐rate, the decreased frequency of mutants at low‐dose‐rate appeared to be accompanied by a shift in genotype toward that of unexposed cells, i.e., in a shift toward a higher frequency of intragenic mutations than was observed with high‐dose‐rate