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    Temperature-sensitive mutations in the Saccharomyces cerevisiae MRT4, GRC5, SLA2 and THS1 genes result in defects in mRNA turnover

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    Authors
    Zuk, Dorit
    Belk, Jonathan Philip
    Jacobson, Allan
    UMass Chan Affiliations
    Department of Molecular Genetics and Microbiology
    Graduate School of Biomedical Sciences
    Document Type
    Journal Article
    Publication Date
    1999-09-03
    Keywords
    Amino Acid Sequence; Carrier Proteins; Cloning, Molecular; Fungal Proteins; *Gene Expression Regulation, Fungal; *Genes, Fungal; Genetic Complementation Test; Half-Life; Molecular Sequence Data; Mutation; Polyribosomes; RNA, Fungal; RNA, Messenger; *RNA-Binding Proteins; Ribosomal Proteins; Saccharomyces cerevisiae; *Saccharomyces cerevisiae Proteins; Suppression, Genetic; Temperature; Threonine-tRNA Ligase
    Life Sciences
    Medicine and Health Sciences
    
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    Link to Full Text
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1460724/
    Abstract
    In a screen for factors involved in mRNA turnover, four temperature-sensitive yeast strains (ts1189, ts942, ts817, and ts1100) exhibited defects in the decay of several mRNAs. Complementation of the growth and mRNA decay defects, and genetic experiments, revealed that ts1189 is mutated in the previously unknown MRT4 gene, ts942 is mutated in GRC5 (encoding the L9 ribosomal protein), ts817 contains a mutation in SLA2 (encoding a membrane protein), and ts1100 contains a mutation in THS1 (encoding the threonyl-tRNA synthetase). Three of the four mutants (mrt4, grc5, and sla2) were not defective in protein synthesis, suggesting that these strains contain mutations in factors that may play a specific role in mRNA decay. The mRNA stabilization observed in the ths1 strain, however, could be due to the significant drop in translation observed in this mutant at 37 degrees. While the three interesting mutants appear to encode novel mRNA decay factors, at least one could be linked to a previously characterized mRNA decay pathway. The growth and mRNA decay defects of ts942 (grc5) cells were suppressed by overexpression of the NMD3 gene, encoding a protein shown to participate in a two-hybrid interaction with the nonsense-mediated decay protein Upf1p.
    Source

    Genetics. 1999 Sep;153(1):35-47.

    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/34015
    PubMed ID
    10471698
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