We have found that many laboratory strains of yeast are defective in galactose metabolism owing to a recessive mutation in the previously characterized nuclear gene, IMP1. This defect leads to a requirement for mitochondrial function for growth on, and metabolism of, galactose. Genetic background affects the degree to which cells are defective. In particular, alleles of GAL3 affect the ability to score the Imp phenotype. We have found that in imp1 strains, transcriptional induction of the galactose inducible genes (GAL1, 2, 7 + 10, MEL1) is normal, but galactose transport is reduced in both rho+ and rho0 cells. This phenotype is normally associated with mutations in GAL2, the galactose permease. Although the growth phenotypes of gal2 and imp1 mutants are distinct, we found that the transformation of imp1 rho0 strains with a plasmid containing the GAL2 gene allows these strains to grow on galactose. Initial genetic analyses did not demonstrate linkage between the GAL2 and IMP1 genes owing to the effects of an unlinked gene on the Imp phenotype. By disrupting the GAL2 gene in an Imp+ background, we have shown that IMP1 and GAL2 segregate as tightly linked genes. Based on these data, we believe that imp1 is a partially defective allele of the GAL2 gene.

• PMID: 1745225
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Journal Article | Research Support, U.S. Gov't, P.H.S.

Authors

Ulery TL, Mangus DA, Jaehning JA

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