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Updated: Aug 13, 2026

A Deep-sequencing-assisted, Spontaneous Suppressor Screen in the Fission Yeast Schizosaccharomyces pombe
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A Deep-sequencing-assisted, Spontaneous Suppressor Screen in the Fission Yeast Schizosaccharomyces pombe

Published on: March 7, 2019

Suppression of a mitotic mutant by tRNA-Ala anticodon mutations that produce a dominant defect in late mitosis

Yuu Kimata1, Mitsuhiro Yanagida

  • 1Department of Gene Mechanisms, Graduate School of Biostudies, Kyoto University. Kitashirakawa-Oiwakecho, Sakyo-ku, Kyoto 606-8501, Japan.

Journal of Cell Science
|May 6, 2004
PubMed

Insights

New fission yeast mutants reveal tRNA

Area of Science:

  • Cell Biology
  • Genetics
  • Molecular Biology

Background:

  • The anaphase-promoting complex/cyclosome (APC/C) is crucial for cell cycle progression.
  • Mutations in essential APC/C subunits cause mitotic defects, including metaphase/anaphase transition problems.
  • Temperature-sensitive mutants like cut9-665 provide tools to study APC/C function.

Purpose of the Study:

  • To identify genes responsible for cold-sensitive phenotypes in Schizosaccharomyces pombe.
  • To elucidate the molecular mechanisms underlying mitotic defects caused by these mutants.
  • To investigate the role of transfer RNA (tRNA) modifications in mitosis.

Main Methods:

  • Isolation and characterization of cold-sensitive mutants (scn1, scn2) suppressing a temperature-sensitive APC/C mutant (cut9-665).
  • Genetic analysis to identify the mutated genes.
  • Molecular analysis of tRNA genes and their anticodon sequences.

Main Results:

  • scn1 and scn2 mutants possess identical substitutions in tRNA-Ala (UGC) genes, altering the anticodon to UGU.
  • This alteration enables tRNA-Ala (UGU) to recognize the ACA threonine codon, potentially producing wild-type Cut9 protein.
  • These tRNA mutants exhibit cold-sensitive phenotypes, mitotic defects, chromosome missegregation, and sensitivity to tubulin poisons.

Conclusions:

  • These findings represent the first identification of transfer RNA (tRNA) mutants causing mitotic defects.
  • The study highlights a novel mechanism linking tRNA function to cell cycle regulation and chromosomal stability.
  • The identified tRNA mutants offer new tools for studying mitosis and the consequences of altered codon recognition.

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