Nonsense codon suppression in fission yeast due to mutations of tRNASer.11 and translation release factor Sup35 (eRF3)
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  • 作者：Reine U. Protacio (1)
    Aaron J. Storey (1)
    Mari K. Davidson (1)
    Wayne P. Wahls (1)

    1. Department of Biochemistry and Molecular Biology     ; University of Arkansas for Medical Sciences ; 4301 West Markham Street (slot 516) ; Little Rock ; AR ; 72205-7199 ; USA
  • 关键词：Genetics ; Molecular biology ; Translation ; Phosphoribosylaminoimidazole carboxylase
  • 刊名：Current Genetics
  • 出版年：2015
  • 出版时间：May 2015
  • 年：2015
  • 卷：61
  • 期：2
  • 页码：165-173
  • 全文大小：1,185 KB
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  • 刊物类别：Biomedical and Life Sciences
  • 刊物主题：Life Sciences
    Microbial Genetics and Genomics
    Microbiology
    Biochemistry
    Cell Biology
    Plant Sciences
    Proteomics
  • 出版者：Springer Berlin / Heidelberg
  • ISSN：1432-0983
文摘
In the fission yeast Schizosaccharomyces pombe, sup9 mutations can suppress the termination of translation at nonsense (stop) codons. We localized sup9 physically to the spctrnaser.11 locus and confirmed that one allele (sup9-UGA) alters the anticodon of a serine tRNA. We also found that another purported allele is not allelic. Instead, strains with that suppressor (renamed sup35-F592S) have a single base pair substitution (T1775C) that introduces an amino acid substitution in the Sup35 protein (Sup35-F592S). Reduced functionality of Sup35 (eRF3), the ubiquitous guanine nucleotide-responsive translation release factor of eukaryotes, increases read-through of stop codons. Tetrad dissection revealed that suppression is tightly linked to (inseparable from) the sup35-F592S mutation and that there are no additional extragenic modifiers. The Mendelian inheritance indicates that the Sup35-F592S protein does not adopt an infectious amyloid state ([PSI +] prion) to affect suppression, consistent with recent evidence that fission yeast Sup35 does not form prions. We also report that sup9-UGA and sup35-F592S exhibit different strengths of suppression for opal stop codons of ade6-M26 and ade6-M375. We discuss possible mechanisms for the variation in suppressibility exhibited by the two alleles.

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