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  • Journal
    Digital Access
    Provider
    Version
    PubMed Central
    v. 1-, 2016-
    TandFonline
    v. 1-, 2016-
  • Article
    Björk GR, Kjellin-Stråby K.
    J Bacteriol. 1978 Feb;133(2):508-17.
    Two tRNA methyltransferase mutants, isolated as described in the accompanying paper (G.R. Björk and K. Kjellin-Stråby, J. Bacteriol. 133:499-207, 1978), are biochemicaaly and genetically characterized. tRNA from mutant IB13 lacks 5-methylaminomethyl-2-thio-uridine in vivo due to a permanently nonfunctional methyltransferase. Thus tRNA from this mutant is a specific substrate for the corresponding tRNA methyltransferase in vitro. In spite of this defect in tRNA, such a mutant is viable. Mutant IB11 is conditionally defective in the biosynthesis of 1-methylguanosine in tRNA due to a temperature-sensitive tRNA (1-methyl-guanosine) methyltransferase. In mutant cells grown at a high temperature, the level of 1-methylguanosine in bulk tRNA is 20% of that of the wild type, demonstrating that in this mutant an 80% deficiency of 1-methylguanosine in tRNA is not lethal. Genetically these two distinct lesions, trmC2, causing 5=methylaminomethyl-2-thio-uridine deficiency, and trmD1, giving a temperature-sensitive tRNA (1-methylguanosine)methyltransferase, are both located between 50 and 61 min on the Escherichia coli chromosome.
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