title: The yeast UME5 gene regulates the stability of meiotic mRNAs in response to glucose.
abstract: We reported previously that early meiotic transcripts are highly unstable. These mRNAs exhibit half-lives of approximately 3 min when expressed during vegetative growth in glucose medium and are stabilized twofold during sporulation in acetate medium. Two genes, UME2 and UME5, that regulate the stability of meiosis-specific transcripts have been identified. The wild-type UME5 gene, which has been analyzed in detail, decreases the stability of all meiotic mRNAs tested approximately twofold when expressed during vegetative growth but has no effect on the half-lives of a number of vegetative mRNAs examined. The UME5 gene is dispensable for mitotic and meiotic development. Cells in which the entire UME5 gene has been deleted are viable, although the generation time is slightly longer and sporulation is less efficient. The UME5 transcript is constitutively expressed, and its stability is not autoregulated. The UME5 gene encodes a predicted 63-kDa protein with homology to the family of CDC28 serine/threonine-specific protein kinases. The kinase activity appears to be central to the function of the UME5 protein, since alteration of a highly conserved amino acid in the kinase domain results in a phenotype identical to that of a ume5 deletion. Genetic epistasis studies suggest that the UME2 and UME5 gene products act in the same pathway to regulate meiotic transcript stability. This pathway is independent of deadenylation and translation, two factors known to be important in regulating mRNA turnover. Significantly, the UME5-mediated destabilization of meiotic mRNAs occurs in glucose- but not in acetate-containing medium. Thus, the UME5 gene appears to participate in a glucose signal transduction pathway governing message stability.
authors.affiliation: Department of Molecular Genetics and Cell Biology, University of Chicago, Illinois 60637.
authors.forename: R T
authors.initials: RT
authors.lastname: Surosky
authors.forename: R
authors.initials: R
authors.lastname: Strich
authors.forename: R E
authors.initials: RE
authors.lastname: Esposito
mesh_terms: D000595:Amino Acid Sequence; D001483:Base Sequence; D003001:Cloning, Molecular; D056850:Cyclin-Dependent Kinase 8; D018844:Cyclin-Dependent Kinases; D004271:DNA, Fungal / Q000302:isolation & purification / Q000378:metabolism; D015966:Gene Expression Regulation, Fungal / Q000187:drug effects; D005800:Genes, Fungal / Q000187:drug effects; D005838:Genotype; D005947:Glucose / Q000494:pharmacology*; D007700:Kinetics; D008540:Meiosis; D008938:Mitosis; D008969:Molecular Sequence Data; D010957:Plasmids; D017346:Protein Serine-Threonine Kinases / Q000096:biosynthesis / Q000235:genetics* / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism*; D015183:Restriction Mapping; D012441:Saccharomyces cerevisiae / Q000235:genetics* / Q000254:growth & development / Q000378:metabolism; D029701:Saccharomyces cerevisiae Proteins; D017386:Sequence Homology, Amino Acid
chemical_list: D004271:DNA, Fungal; D012333:RNA, Messenger; D029701:Saccharomyces cerevisiae Proteins; D017346:Protein Serine-Threonine Kinases; D056850:Cyclin-Dependent Kinase 8; D018844:Cyclin-Dependent Kinases; C498309:SSN3 protein, S cerevisiae; D005947:Glucose