Null mutations in the SNF3 gene of Saccharomyces cerevisiae cause a different phenotype than do previously isolated missense mutations.
Missense mutations in the SNF3 gene of Saccharomyces cerevisiae were previously found to cause defects in both glucose repression and derepression of the SUC2 (invertase) gene. In addition, the growth properties of snf3 mutants suggested that they were defective in uptake of glucose and fructose. We have cloned the SNF3 gene by complementation and demonstrated linkage of the cloned DNA to the chromosomal SNF3 locus. The gene encodes a 3-kilobase poly(A)-containing RNA, which was fivefold more abundant in cells deprived of glucose. The SNF3 gene was disrupted at its chromosomal locus by several methods to create null mutations. Disruption resulted in growth phenotypes consistent with a defect in glucose uptake. Surprisingly, gene disruption did not cause aberrant regulation of SUC2 expression. We discuss possible mechanisms by which abnormal SNF3 gene products encoded by missense alleles could perturb regulatory functions.
D003001:Cloning, Molecular; D004794:Enzyme Repression; D005796:Genes; D005800:Genes, Fungal; D005809:Genes, Regulator; D005947:Glucose / Q000378:metabolism; D006026:Glycoside Hydrolases / Q000096:biosynthesis / Q000235:genetics; D009154:Mutation; D010641:Phenotype; D010957:Plasmids; D012441:Saccharomyces cerevisiae / Q000201:enzymology / Q000235:genetics* / Q000254:growth & development; D043324:beta-Fructofuranosidase
D006026:Glycoside Hydrolases; D043324:beta-Fructofuranosidase; D005947:Glucose