Further characterization of the yeast pso4-1 mutant: interaction with rad51 and rad52 mutants after photoinduced psoralen lesions
| Autor: | João Antonio Pêgas Henriques, Elisabete José Vicente, J. Brozmanová, Ana Clara Guerrini Schenberg, Marcos Antonio de MoraisJunior |
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| Rok vydání: | 1996 |
| Předmět: |
Saccharomyces cerevisiae Proteins
DNA Repair DNA repair Ultraviolet Rays Mutant Genes Fungal RAD51 Mutagenesis (molecular biology technique) Saccharomyces cerevisiae Biology Homology directed repair Fungal Proteins Genetics DNA Fungal Replication protein A Recombination Genetic Genetic Complementation Test Epistasis Genetic General Medicine DNA repair protein XRCC4 Molecular biology Rad52 DNA Repair and Recombination Protein DNA-Binding Proteins Mutagenesis Mutation Methoxsalen Rad51 Recombinase Nucleotide excision repair Plasmids |
| Zdroj: | Current genetics. 29(3) |
| ISSN: | 0172-8083 |
| Popis: | The pso4-1 mutant was characterized as deficient in some types of recombination, including gene conversion, crossing over, and intrachromosomal recombination. The mode of interaction between pso4-1 and rad51 and between pso4-1 and rad52 mutants indicated that the PSO4 gene belongs to the RAD52 epistasis group for strand-break repair. Moreover, the presence of the pso4-1 mutation decreased 8-MOP-photoinduced mutagenesis of the rad51 and rad52 mutants. Complementation tests using heterozygous diploid strains showed that the pso4 protein might interact with the rad52 protein during repair of 8-mop photolesions. The pso4-1 mutant, even though defective in inter- and intra-chromosomal recombination, conserves the ability for plasmid integration of circular and linear plasmid DNA. On the other hand, similar to the rad51 mutant, pso4-1 was able to incise but did not restore high-molecular-weight DNA during the repair of cross links induced by 8-MOP plus UVA. These results, together with those of previous reports, indicate that the PSO4 gene belongs to the RAD52 DNA repair group and its product participates in the DNA rejoining step of the repair of cross-link lesions, which are crucial for induced mutagenesis and recombinogenesis. |
| Databáze: | OpenAIRE |
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