Effects of mevinolin on cell cycle progression and viability of tobacco BY-2 cells

Authors

  • Andréa Hemmerlin,

    1. Centre National de la Recherche Scientifique, Institut de Biologie Moléculaire des Plantes, Département d’Enzymologie Cellulaire et Moléculaire, Institut de Botanique, Université Louis Pasteur, 28 rue Goethe, F-67083 Strasbourg, France
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  • Thomas J. Bach

    Corresponding author
    1. Centre National de la Recherche Scientifique, Institut de Biologie Moléculaire des Plantes, Département d’Enzymologie Cellulaire et Moléculaire, Institut de Botanique, Université Louis Pasteur, 28 rue Goethe, F-67083 Strasbourg, France
      *For correspondence (fax +33 3 88 35 84 84;
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  • This manuscript is dedicated to the late Dr Claude Gigot, our colleague and friend.

*For correspondence (fax +33 3 88 35 84 84;

Summary

Mevinolin, an inhibitor of 3-hydroxy-3-methylglutaryl-CoA reductase, was used to study the importance of mevalonic acid (MVA) for cell cycle progression of tobacco (Nicotiana tabacum L.) BY-2 cells. After treatment with 5 μM mevinolin, the cell cycle progression was completely blocked and two cell populations accumulated (80% in phase G0/G1 and 20% in G2/M). The arrest could be released by subsequent addition of MVA. Effects were compared to those caused by aphidicolin, an inhibitor of α-like DNA polymerases that blocks cell cycle at the entry of the S phase. The 80% proportion of mevinolin-treated TBY-2 cells was clearly arrested before the aphidicolin-inducible block. By the aid of a double-blocking technique, it was shown that the mevinolin-induced cell arrest of highly synchronized cells was due to interaction with a control point located at the mitotic telophase/entry G1 phase. Depending on the developmental stage, mevinolin induced rapid cell death in a considerable percentage of cells. Mevinolin treatment led to a partial synchronization, as shown by the increase in mitotic index. The following decrease was correlated with the above-mentioned induction of cell death.

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