Genetic and molecular characterization of GAL83: its interaction and similarities with other genes involved in glucose repression in Saccharomyces cerevisiae

• Published in: Genetics (Austin) 1993-11, Vol.135 (3), p.655-664
• Main Authors: Erickson, J.R, Johnston, M
• Format: Article
• Language: English
• Subjects: Alleles; Amino Acid Sequence; AMP-Activated Protein Kinases; Base Sequence; Biological and medical sciences; DNA, Fungal - genetics; Fundamental and applied biological sciences. Psychology; Fungal Proteins - genetics; GENE; Gene Expression Regulation, Fungal; GENES; Genes, Fungal - drug effects; Genes. Genome; Genetic Complementation Test; GENETICA; GENETIQUE; GLUCOSA; GLUCOSE; Glucose - metabolism; Glucose - pharmacology; INTERACCION DE GENES; INTERACTION GENIQUE; Investigations; METABOLISME DES GLUCIDES; METABOLISMO DE CARBOHIDRATOS; Molecular and cellular biology; Molecular genetics; Molecular Sequence Data; MUTACION INDUCIDA; Mutation; MUTATION PROVOQUEE; Phenotype; PROTEINA QUINASA; PROTEINAS; PROTEINE; PROTEINE KINASE; Repressor Proteins; Restriction Mapping; SACCHAROMYCES CEREVISIAE; Saccharomyces cerevisiae - drug effects; Saccharomyces cerevisiae - genetics; Saccharomyces cerevisiae - metabolism; Saccharomyces cerevisiae Proteins; SECUENCIA NUCLEICA; Sequence Homology, Amino Acid; SEQUENCE NUCLEIQUE
• ISSN: 0016-6731; 1943-2631; 1943-2631
• DOI: 10.1093/genetics/135.3.655

Expression of the GAL genes of Saccharomyces cerevisiae is subject to glucose repression, a global regulatory mechanism that requires several gene products. We have isolated GAL83, one of these genes required for glucose repression. The sequence of the predicted Gal83 protein is homologous to two other yeast proteins, Sip1p and Sip2p, which are known to interact with the SNF1 gene product, a protein kinase required for expression of the GAL genes. High-copy clones of SIP1 and SIP2 cross-complement the GAL83-2000 mutation (as well as GAL82-1, a mutation in another gene involved in glucose repression), suggesting that these four genes may perform similar functions in glucose repression. Consistent with this hypothesis, a gal83 null mutation does not affect glucose repression, and only dominant or partially dominant mutations exist in GAL83 (and GAL82). Two other observations were made that suggests that GAL83 functions interdependently with GAL82 and REG1 (another gene involved in glucose repression) to effect glucose repression: 1) REG1 on a lowcopy plasmid cross-complements GAL82-1 and GAL83-2000 mutations, and 2) all pairwise combinations of reg1, GAL82-1 and GAL83-2000 fail to complement one another. Such unlinked noncomplementation suggests that Gal83p, Gal82p and Reg1p may interact with one another. Possible roles for GAL83, GAL82 and REG1 are discussed in relation to SNF1, SIP1 and SIP2