Induction of mutations in Saccharomyces cerevisiae by ultraviolet light

Abstract

Mutation induction by ultraviolet light was examined in a UV-sensitive ( uvs 9-3) and a wild-type ( UVS) strain. Induced reversion to prototrophy in both strains occurred regardless of whether the original auxotrophic mutation arose by a base-pair substitution (missense or nonsense category) or by an addition-deletion event. In the UVS strain a significant amount of the UV-induced reversional lesions were due to pyrimidine dimers while in the sensitive strain pyrimidine dimer damage was only detected when reversion occurred by addition-deletion events. At equal doses, UV-induced reversion frequencies in the UVS strain were always less than in the uvs 9-3 strain. A comparison of dark repair and photoreaction of lethal and mutational damage indicated that lethal lesions are generally repaired more readily than mutational lesions by dark repair. Similarly, photoreactivation removes lethal damage in the uvs strain mor efficiently than mutational damage; however, in the wild-type strain both types of damage are removed with equal efficiency. Forward mutations induced at the tr 5 locus were classified according to ability to complement, suppressibility and osmotic remediability. A mutant exhibiting any one of these characteristics was considered to have arisen by a base-pair substitution event. After UV 16 tr 5 mutants (among 42233 colonies) were isolated in the uvs strain without photoreactivation, while none were isolated after photoreactivation (0/23541 colonies). Twelve of the mutants were attributed to base-pair substitution events; thus, pyrimidine dimers were concluded to cause primarily base-pair susbstitution mutations at this locus. Since the mutation frequency at the tr 5 locus in the UVS strain was the same before and after photoreactivation, the lesions causing the mutations were considered to be those other than pyrimidine dimers. However, this damage also produced mainly base-pair substitution mutations ( 16 19 ). The production of whole colony and sectored mutants for several loci was also examined in the uvs 9-3 and the UVS strains. It is proposed that whole colony mutants arise by dark repair acting in some way on the DNA strand opposite the mutational lesion.