Fredericamycin A Affects Mitochondrial Inheritance and Morphology in Saccharomyces cerevisiae

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  • IMAMURA Yuko
    Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University
  • YUKAWA Masashi
    Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University
  • KIMURA Ken-ichi
    Department of Agro-bioscience, Faculty of Agriculture, Iwate University
  • TAKAHASHI Hidetoshi
    Research Institute of Life Science, Snow Brand Milk Products Co., Ltd.
  • SUZUKI Yoshihiro
    Department of Applied Molecular Bioscience, Graduate School of Bioagricultural Sciences, Nagoya University
  • OJIKA Makoto
    Department of Applied Molecular Bioscience, Graduate School of Bioagricultural Sciences, Nagoya University
  • SAKAGAMI Youji
    Department of Applied Molecular Bioscience, Graduate School of Bioagricultural Sciences, Nagoya University
  • TSUCHIYA Eiko
    Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University

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  • Fredericamycin A Affects Mitochondrial Inheritance and Morphology in<i>Saccharomyces cerevisiae</i>

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Fredericamycin A (FMA) is an antibiotic product of Streptomyces griseus that exhibits modest antitumor activity in vivo and in vitro, but, its functions in vivo are poorly understood. We identified this compound as an inducer of G1 arrest in the yeast, Saccharomyces cerevisiae. FMA exhibits an IC50 of 24 nM towards the growth of a disruptant of multi-drug resistance genes, W303-MLC30, and its cytotoxicity is a function of the time of exposure as well as drug dose. Addition of 0.8 μM of FMA caused aggregation of mitochondria within 10 min of incubation and the drug induced petites at high frequency after 4 h of incubation. rho− cells were about 20 times more resistant to FMA than isogenic rho+ cells. Overexpression of topoisomerase I, a previously suggested target of the drug, did not alleviate the sensitivity of the cells to FMA or the aggregation of mitochondria. Our results suggest that mitochondria are the primary target site of FMA.

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