title: Accumulation of recessive lethal mutations in Saccharomyces cerevisiae mlh1 mismatch repair mutants is not associated with gross chromosomal rearrangements.
abstract: We examined mismatch repair (MMR)-defective diploid strains of budding yeast grown for approximately 160 generations to determine whether decreases in spore viability due to the uncovering of recessive lethal mutations correlated with an increase in gross chromosomal rearrangements (GCRs). No GCRs were detected despite dramatic decreases in spore viability, suggesting that frameshift and/or other unrepaired DNA replication lesions play a greater role than chromosomal instability in decreasing viability in MMR-defective strains.
authors.affiliation: Department of Molecular Biology and Genetics, Cornell University, Ithaca, New York 14853-2703, USA.
authors.forename: Julie Akiko
authors.initials: JA
authors.lastname: Heck
authors.forename: David
authors.initials: D
authors.lastname: Gresham
authors.forename: David
authors.initials: D
authors.lastname: Botstein
authors.forename: Eric
authors.initials: E
authors.lastname: Alani
mesh_terms: D048868:Adaptor Proteins, Signal Transducing; D020137:Base Pair Mismatch / Q000235:genetics*; D002470:Cell Survival / Q000235:genetics; D002869:Chromosome Aberrations; D016368:Frameshift Mutation / Q000502:physiology; D005656:Fungal Proteins / Q000235:genetics*; D015321:Gene Rearrangement / Q000502:physiology; D005804:Genes, Lethal / Q000502:physiology; D005808:Genes, Recessive / Q000502:physiology; D008954:Models, Biological; D000070957:MutL Protein Homolog 1; D009154:Mutation / Q000502:physiology*; D009693:Nucleic Acid Hybridization / Q000379:methods; D011336:Probability; D012441:Saccharomyces cerevisiae / Q000235:genetics*; D029701:Saccharomyces cerevisiae Proteins
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D005656:Fungal Proteins; C088859:MLH1 protein, S cerevisiae; D029701:Saccharomyces cerevisiae Proteins; D000070957:MutL Protein Homolog 1