Abstract
A cytoplasmic mutant of Aspergillus nidulans produced two classes of conidia, mutant and non-mutant. The mutant conidia were more resistant to u.v. than the non-mutant, and this difference was shown to be attributable entirely to the cytoplasm. There were no differences between the two classes on gamma-irradiation. It was not practicable to examine the possibility of differences in a cytoplasmic target in this system, and an attempt was made to test whether cytoplasmically determined differences in repair capacity might account for the different u.v. sensitivities. The chemical inhibitors of repair processes, acriflavine and caffeine, which are effective in some bacteria did not reduce but enhanced survival in the fungus. Some other treatments which enhanced survival also delayed germination, and an explanation based on a prolonged period for repair is suggested.