title: [Interaction of gene HSM3 with genes of the epistatic RAD6 group in yeast Saccharomyces cerevisiae].
abstract: In eukaryotes, damage tolerance of matrix DNA is mainly determined by the repair pathway under the control of the RAD6 epistatic group of genes. T this pathway is also a main source of mutations generated by mutagenic factors. The results of our recent studies show that gene HSM3 participating in the control of adaptive mutagenesis increases the frequency of mutations induced by different mutagens. Mutations rad18, rev3, and mms2 controlling various stages of the RAD6 pathway are epistatic with mutation hsm3 that decreases UV-induced mutagenesis to the level typical for single radiation-sensitive mutants. The level of mutagenesis in the double mutant srs2 hsm3 was lower than in both single mutants. Note that a decrease in the level of mutagenesis relative to the single mutant srs2 depends on the mismatch repair, since this level in the triple mutant srs2 hsm3 pms 1 corresponds to that in the single mutant srs2. These data show that the mutator phenotype hsm3 is probably determined by processes occurring in a D loop. In a number of current works, the protein Hsm3 was shown to participate in the assembly of the proteasome complex S26. The assembly of proteasomes is governed by the N-terminal domain. Our results demonstrated that the Hsm3 protein contains at least two domains; the N-terminal part of the domain is responsible for the proteasome assembly, whereas the C-terminal portion of the protein is responsible for mutagenesis.
authors.forename: A Iu
authors.initials: AIu
authors.lastname: Chernenkov
authors.forename: L M
authors.initials: LM
authors.lastname: Gracheva
authors.forename: T A
authors.initials: TA
authors.lastname: Evstiukhina
authors.forename: S V
authors.initials: SV
authors.lastname: Koval'tsova
authors.forename: V T
authors.initials: VT
authors.lastname: Peshekhonov
authors.forename: I V
authors.initials: IV
authors.lastname: Fedorova
authors.forename: V G
authors.initials: VG
authors.lastname: Korolev
mesh_terms: D004260:DNA Repair / Q000528:radiation effects; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism; D004259:DNA-Directed DNA Polymerase / Q000235:genetics / Q000378:metabolism; D004843:Epistasis, Genetic / Q000502:physiology / Q000528:radiation effects*; D018832:Molecular Chaperones / Q000235:genetics / Q000378:metabolism*; D016296:Mutagenesis / Q000528:radiation effects*; D009154:Mutation; D046988:Proteasome Endopeptidase Complex / Q000235:genetics / Q000378:metabolism; D017434:Protein Structure, Tertiary; D012441:Saccharomyces cerevisiae / Q000235:genetics / Q000378:metabolism*; D029701:Saccharomyces cerevisiae Proteins / Q000235:genetics / Q000378:metabolism*; D044763:Ubiquitin-Conjugating Enzymes / Q000235:genetics / Q000378:metabolism*; D044767:Ubiquitin-Protein Ligases / Q000235:genetics / Q000378:metabolism; D014466:Ultraviolet Rays
chemical_list: D004268:DNA-Binding Proteins; C112193:HSM3 protein, S cerevisiae; C112520:MMS2 protein, S cerevisiae; D018832:Molecular Chaperones; C063607:RAD18 protein, S cerevisiae; D029701:Saccharomyces cerevisiae Proteins; C471606:RAD6 protein, S cerevisiae; D044763:Ubiquitin-Conjugating Enzymes; D044767:Ubiquitin-Protein Ligases; D004259:DNA-Directed DNA Polymerase; C092602:REV3 protein, S cerevisiae; D046988:Proteasome Endopeptidase Complex