involvement of the RAD6 gene in starvation-induced reverse mutation in Saccharomyces cerevisiae

The accumulation of Ade+ revertants during adenine starvation and Trp+ revertants during tryptophan starvation in haploid polyauxotrophic strains of Saccharomyces cerevisiae occurs in a time-dependent manner. Accumulation of revertants is enhanced in Rad6- strains, suggesting that starvation-induced...

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Bibliographic Details
Published in:Molecular & general genetics 1998-06, Vol.258 (5), p.546-552
Main Authors: Storchova, Z, Rojas Gil, A.P, Janderova, B, Vondrejs, V
Format: Article
Language:English
Subjects:
adaptation
Adaptation, Physiological - genetics
adaptive mutations
adenine
Adenine - metabolism
genes
Genes, Fungal - physiology
genetic change
growth
Ligases - genetics
Ligases - physiology
Mutation
nutrient deficiencies
Phenotype
reversion
revertants
Saccharomyces cerevisiae
Saccharomyces cerevisiae - genetics
Saccharomyces cerevisiae - growth & development
Saccharomyces cerevisiae Proteins
tryptophan
Tryptophan - metabolism
Ubiquitin-Conjugating Enzymes
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Summary:The accumulation of Ade+ revertants during adenine starvation and Trp+ revertants during tryptophan starvation in haploid polyauxotrophic strains of Saccharomyces cerevisiae occurs in a time-dependent manner. Accumulation of revertants is enhanced in Rad6- strains, suggesting that starvation-induced reversion is influenced by some of the RAD6 gene functions. The higher frequency of adaptive reversions in Rad6- strains is somewhat influenced by, but does not totally depend on, the genetic background. Therefore, the RAD6 gene product is involved in maintaining a low level not only of spontaneous mutation but also of starvation-induced reversion. The starvation-induced Ade+ and Trp+ reversions both appear to be adaptive. The analysis of growth characteristics and the genotype of revertants shows a difference between early and late-appearing revertants. These results support the hypothesis that the adaptivity of starvation-induced reversion is based on the selective fixation of random mutations, and particularly on transcription-enhanced repair and/or mutagenesis processes.
ISSN:0026-8925
1432-1874
DOI:10.1007/s004380050766