Interactions among mutations affecting spontaneous mutation, mitotic recombination, and DNA repair in yeast

• Published in: Current genetics Vol. 27; no. 2; p. 102
• Main Authors: Montelone, B.A, Koelliker, K.J. (Kansas State Univ., Manhattan (USA). Div. of Biology)
• Format: Journal Article
• Language: English
• Published: United States 1995
• Subjects: Adenosine Triphosphatases - genetics; Adenosine Triphosphatases - metabolism; ADN; DNA Helicases - genetics; DNA Helicases - metabolism; DNA Repair; DNA, Fungal; DNA-Binding Proteins - genetics; DNA-Binding Proteins - metabolism; Fungal Proteins - genetics; Fungal Proteins - metabolism; Fungal Proteins - physiology; GENE; GENES; Hyper-recombination mutants; Ligases - genetics; Ligases - metabolism; MITOSE; MITOSIS; MUTANT; MUTANTES; Mutation; Mutators; NUCLEOTIDE; Nucleotide excision repair; NUCLEOTIDOS; Pflanzenzuechtung; Rad52 DNA Repair and Recombination Protein; RECOMBINACION; RECOMBINAISON; Recombination, Genetic; SACCHAROMYCES CEREVISIAE; Saccharomyces cerevisiae - genetics; Saccharomyces cerevisiae - metabolism; Saccharomyces cerevisiae Proteins; SECUENCIA NUCLEOTIDICA; SEQUENCE NUCLEOTIDIQUE; Ubiquitin-Conjugating Enzymes
• ISSN: 0172-8083; 1432-0983
• DOI: 10.1007/BF00313423

The mutant alleles mms9-1, mms13-1, or mms21-1 of Saccharomyces cerevisiae confer pleiotropic effects, including sensitivity to the alkylating agent methyl methanesulfonate, elevations in spontaneous mutation and mitotic recombination, defects in meiosis, and cross-sensitivity to radiation. Double-mutant strains were constructed containing an mms mutation and a defect in either excision repair, mutagenic repair, or recombinational repair and measured the levels of spontaneous mutation and mitotic reombination. Double mutants lacking excision repair show elevations in spontaneous mutation but with predominantly unchanged levels of mitotic recombination. RAD52 function was required for the expression of the hyper-recombination phenotype of the mms9-1, mms13-1, and mms21-1 alleles; double mutants displayed the very low recombination levels characteristic of rad52 mutants. Phenotypes of double mutants containing one of the mms alleles and either of the hyper-recombination/mutator rad6-1 or rad3-102 alleles suggest that the mutagenic lesions in mms strains may not be identical to the recombinogenic lesions.