Current Genetics

, Volume 29, Issue 3, pp 211–218

Further characterization of the yeastpso4-1 mutant: interaction withrad51 andrad52 mutants after photoinduced psoralen lesions

Authors

  • Marcos Antonio de MoraisJunior
    • Departamento de Biofisica e Centro de BiotecnologiaUFRGS
  • Elisabete José Vicente
    • Departamento de Microbiologia, Instituto de Ciências Biomédicas, USPCidade Universitária
  • Jela Brozmanova
    • Department of Molecular Genetic, Cancer Research InstituteSlovak Academy of Sciences
  • Ana Clara Guerrini Schenberg
    • Departamento de Microbiologia, Instituto de Ciências Biomédicas, USPCidade Universitária
  • João Antonio Pegas Henriques
    • Departamento de Biofisica e Centro de BiotecnologiaUFRGS
Original Paper

DOI: 10.1007/BF02221550

Cite this article as:
de Morais, M.A., Vicente, E.J., Brozmanova, J. et al. Curr Genet (1996) 29: 211. doi:10.1007/BF02221550

Abstract

Thepso4-1 mutant was characterized as deficient in some types of recombination, including gene conversion, crossing over, and intrachromosomal recombination. The mode of interaction betweenpso4-1 andrad51 and betweenpso4-1 andrad52 mutants indicated that thePSO4 gene belongs to theRAD52 epistasis group for strand-break repair. Moreover, the presence of thepso4-1 mutation decreased 8-MOP-photoinduced mutagenesis of therad51 andrad52 mutants. Complementation tests using heterozygous diploid strains showed that thePso4 protein might interact with theRad52 protein during repair of 8-MOP photolesions. Thepso4-1 mutant, even though defective in inter- and intea-chromosomal recombination, conserves the ability for plasmid integration of circular and linear plasmid DNA. On the other hand, similar to therad51 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 thePSO4 gene belongs to theRAD52 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.

Key words

pso4-1 mutantRecombinational repairDouble-strand breaksMutagenesis8-methoxypsoralen
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© Springer-Verlag 1996