A novel class of Saccharomyces cerevisiae mutants specifically UV-sensitive to “petite” induction
- 1 January 1976
- journal article
- research article
- Published by Springer Nature in Molecular Genetics and Genomics
- Vol. 148 (3) , 251-261
- https://doi.org/10.1007/bf00332899
Abstract
A mutant of Saccharomyces cerevisiae has been isolated which, though exhibiting a normal response to nuclear genetic damage by ultraviolet light (UV), is more sensitive than its wild type specifically in the production of the cytoplasmic (rho -) mutation by this agent. Some of the features of this mutation which has been designated uvsρ5 are: The mutation is recessive, it exhibits a Mendelian, and hence presumably nuclear, pattern of segregation, but manifests its effects specifically and pleiotropically on mitochondrial functions. Mutant cells resemble their wild type parents in a) growth characteristics on glucose; b) in their UV induced dose response to lethality or nuclear mutation and c) the ability of their mitochondrial genome, upon mating with appropriate testers, of transmitting and recombining various markers, albeit with enhanced efficiency. Similarly, d) they are able to modulate the expression of mitochondrial mutagenesis by ethidium bromide. Thus their mitochondrial DNA appears genetically as competent as that of the wild type. Mutant cells differ from their wild type parents in a) growth characteristics on glycerol; b) susceptibility to induction of the mitochondrial (rho -) mutation by various mutagens, in that the rate of spontaneous mutation is slightly and that by UV is significantly enhanced, while that by ethidium bromide is greatly diminished. Conversely, c) modulating influences resulting in the repair of initial damage are diminished for UV and stimulated in the case of Berenil. The amount of mitochondrial DNA per cell appears elevated in the mutant, relative to wild type, and its rate of degradation subsequent to a mutagenic exposure to either UV or ethidium bromide is diminished. A self-consistent scheme to account for this and all other information so far available for the induction and modulation of the (rho -) mutation is presented.This publication has 42 references indexed in Scilit:
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