Essential roles of Snf21, a Swi2/Snf2 family chromatin remodeler, in fission yeast mitosis

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  • Yamada Kentaro
    Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo Cellular and Molecular Biology Laboratory, RIKEN Discovery Research Institute Division of Molecular and Cellular Physiology, International Graduate School of Arts and Sciences, Yokohama City University
  • Hirota Kouji
    Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo Cellular and Molecular Biology Laboratory, RIKEN Discovery Research Institute
  • Mizuno Ken-ichi
    Genome Damage and Stability Centre, University of Sussex
  • Shibata Takehiko
    Cellular and Molecular Biology Laboratory, RIKEN Discovery Research Institute Division of Molecular and Cellular Physiology, International Graduate School of Arts and Sciences, Yokohama City University
  • Ohta Kunihiro
    Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo Cellular and Molecular Biology Laboratory, RIKEN Discovery Research Institute

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ATP-dependent chromatin remodelers (ADCRs) convert local chromatin structure into both transcriptional active and repressive state. Recent studies have revealed that ADCRs play diverse regulatory roles in chromosomal events such as DNA repair and recombination. Here we have newly identified a fission yeast gene encoding a Swi2/Snf2 family ADCR. The amino acid sequence of this gene, snf21+, implies that Snf21 is a fission yeast orthologue of the budding yeast Sth1, the catalytic core of the RSC chromatin remodeling complex. The snf21+ gene product is a nuclear protein essential to cell viability: the null mutant cells stop growing after several rounds of cell divisions. A temperature sensitive allele of snf21+, snf21-36 exhibits at non-permissive temperature (34°C) a cell cycle arrest at G2-M phase and defects in chromosome segregation, thereby causing cell elongation, lack of cell growth, and death of some cell population. snf21-36 shows thiabendazole (TBZ) sensitivity even at permissive temperature (25°C). The TBZ sensitivity becomes severer as snf21-36 is combined with the deletion of a centromere-localized Mad2 spindle checkpoint protein. The cell cycle arrest phenotype at 34°C cannot be rescued by the mad2+ deletion, although it is substantially alleviated at 30°C in mad2Δ. These data suggest that Snf21 plays an essential role in mitosis possibly functioning in centromeric chromatin.<br>

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