The rate of nuclear fusion (karyogamy) in the haploid smut fungus, Ustilago violacea, designated D, can be determined accurately from the frequency of diploid formation. The spontaneous value of D depends mainly on the age of the cells and the temperature, varying from 10-5 to 10-2. Ultraviolet light (u.v., 254 nm) induces high rates of fusion, up to 100 % of the survivors being diploid after very high doses. That this increase is caused by induction and not by selection is shown by the absolute increase in the number of diploids obtained under some conditions. The high value of D after a u.v. treatment is reduced by conditions which favour photoreactivation or dark repair. Acriflavine, an inhibitor of dark repair, maintains high values of D, while caffeine which also inhibits dark repair abolishes the u.v. induction entirely.
Ultraviolet-sensitive mutants located at 4 loci were tested for their effect on spontaneous and u.v.-induced karyogamy. One mutant (uvs4) showed complete absence of somatic karyogamy even after high doses of ultraviolet. Mutant uvs2 had no effect on the value of D, while mutants uvs1 and uvs3 showed low spontaneous karyogamy, but could be induced by low doses of u.v. to yield large numbers of diploids.
It is suggested that an inhibitor of karyogamy is formed in somatic cells and destroyed prior to premeiotic karyogamy. The accuracy of the transcription of this inhibitor seems to be impaired by ultraviolet, but can be restored following DNA repair. The absence of somatic karyogamy in uvs4 mutants may indicate that these strains contain an altered organelle involved in the control of karyogamy, e.g. the spindle pole body situated on the nuclear membrane, and known to contain DNA. Alteration of such an organelle could produce pleiotropic effects including u.v. sensitivity and inhibitor production or action.