Publications by authors named "A Iu Chernenkov"

In the Saccharomyces cerevisiae yeasts, the DOT1 gene product provides methylation of lysine 79 (K79) of hi- stone H3 and the SET2 gene product provides the methylation of lysine 36 (K36) of the same histone. We determined that the dot1 and set2 mutants suppress the UV-induced mutagenesis to an equally high degree. The dot1 mutation demonstrated statistically higher sensitivity to the low doses of MMC than the wild type strain.

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Long-term storage at +4 degrees C and cultivation at +30 degrees C changes the spontaneous mutation rate of the yeast Saccharomyces cerevisiae double mutants rad52hsm3delta and rad52hsm6-1. Combinations of hsm3 and hsm6 mutations with the rad52 mutation lead to a decrease of the spontaneous mutation rate mediated by DNA repair synthesis in multiply replanted strains in comparison with the same strains investigated right after RAD52 gene decay. Combinations of hsm3 and hsm6 mutations with mutations in other genes of the RAD52 epistatic group did not provide a spontaneous mutation rate decrease.

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SIN3 gene product operates as a repressor for a huge amount of genes in Saccharomyces cerevisiae. Sin3 protein with a mass of about 175 kDa is a member of the RPD3 protein complex with an assessed mass of greater than 2 million Da. It was previously shownthat RPD3 gene mutations influence recombination and repair processes in S.

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Previously, we isolated mutant yeasts Saccharomyces cerevisiae with an increased rate of spontaneous mutagenesis. Here, we studied the properties of HSM6 gene, the hsm6-1 mutation of which increased the frequency of UV-induced mutagenesis and decreased the level of UV-induced mitotic crossover at the centromere gene region, ADE2. HSM6 gene was mapped on the left arm of chromosome 11 in the region where the PSY4 gene is located.

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It was assumed previously that the mutator phenotype of the hms3 mutant was determined by processes taking place in the D-loop. As a next step, genetic analysis was performed to study the interactions between the hsm3 mutation and mutations of the genes that control the initial steps of the D-loop formation. The mutations of the MMS4 and XRS2 genes, which initiate the double-strand break formation and subsequent repair, were shown to completely block HSM3-dependent UV-induced mutagenesis.

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