Ploidy level and mutation to hypoxanthine-guanine-phosphoribosyl-transferase (HGPRT) deficiency in Chinese hamster cells.

The X-ray induction of 8-azaguanine (AG) resistent mutants in two sets of diploid and tetraploid Chinese hamster cells (DON and V79) was investigated. It was found that (i) the induced mutant frequencies in diploid and tetraploid cells appeared to be of the same order of magnitude and (ii) all mutants showed almost complete loss of hypoxanthine-guanine-phosphoribosyl-transferase (HGPRT) activity except that in the tetraploid V79 cells 50--100% of activity was retained. The gene--dosage effect for glucose-6-phosphate dehydrogenase (G6PD) in these cells make it possible to determine the number of chromosomes bearing the HGPRT-gene in mutants by measuring the G6PD activity per cell. The results show that the spontaneous and induced mutants from the diploid V79 and DON as well as the tetraploid DON cells retained the G6PD activity of the parental cells, whereas the induced mutants from the tetraploid V79 cells had about 35% of the parental G6PD activity. With 6-thioguanine (TG) as selective agent, the induced mutant frequencies in diploid and tetraploid DON cells and in diploid V79 cells appeared to be of the same order of magnitude but no mutants could be recovered from tetraploid V79 cells in a single step. TG-resistant tetraploid V79 cells could only be obtained from the AG-resistant mutants after a second selection. The HGPRT activity was lost in these mutants and some of them showed an increase in G6PD activity. The combined data cannot be explained on the basis of a single genetic mechanism.