Participation of the HIM1 gene of yeast Saccharomyces cerevisiae in the error-free branch of post-replicative repair and role Polη in him1-dependent mutagenesis
Autor: | V. T. Peshekhonov, V. G. Korolev, E. A. Alekseeva, T. A. Evstyukhina |
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Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
DNA Replication
Saccharomyces cerevisiae Proteins DNA Repair DNA damage Saccharomyces cerevisiae DNA-Directed DNA Polymerase Biology medicine.disease_cause 03 medical and health sciences Post-replication repair Genetics medicine Postreplication repair Gene HIM1 gene 030304 developmental biology 0303 health sciences Mutation 030302 biochemistry & molecular biology Mutagenesis Recombinational DNA Repair Epistasis Genetic General Medicine biology.organism_classification Yeast Cell biology Proliferating cell nuclear antigen Ubiquitin-Conjugating Enzymes biology.protein Original Article Homologous recombination |
Zdroj: | Current Genetics |
ISSN: | 1432-0983 0172-8083 |
Popis: | In eukaryotes, DNA damage tolerance (DDT) is determined by two repair pathways, homologous repair recombination (HRR) and a pathway controlled by the RAD6-epistatic group of genes. Monoubiquitylation of PCNA mediates an error-prone pathway, whereas polyubiquitylation stimulates an error-free pathway. The error-free pathway involves components of recombination repair; however, the factors that act in this pathway remain largely unknown. Here, we report that theHIM1gene participates in error-free DDT. Notably, inactivationRAD30gene encoding Polη completely suppresseshim1-dependent UV mutagenesis. Furthermore, data obtained show a significant role of Polη inhim1-dependent mutagenesis, especially at non-bipyrimidine sites (NBP sites). We demonstrate thathim1mutation significantly reduces the efficiency of the induction expression ofRNRgenes after UV irradiation. Besides, this paper presents evidence that significant increase in the dNTP levels suppresshim1-dependent mutagenesis. Our findings show that Polη responsible forhim1-dependent mutagenesis. |
Databáze: | OpenAIRE |
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