c-Mos forces the mitotic cell cycle to undergo meiosis II to produce haploid gametes

  1. Kazunori Tachibana*,
  2. Daisuke Tanaka*,
  3. Tomohiro Isobe*, and
  4. Takeo Kishimoto*,,
  1. *Laboratory of Cell and Developmental Biology, Graduate School of Bioscience, Tokyo Institute of Technology, and Core Research for Evolutional Science and Technology Research Project, Japan Science and Technology Corporation, Nagatsuta 4259, Midoriku, Yokohama 226-8501, Japan
  1. Communicated by Joan V. Ruderman, Harvard Medical School, Boston, MA (received for review August 11, 2000)

Abstract

The meiotic cycle reduces ploidy through two consecutive M phases, meiosis I and meiosis II, without an intervening S phase. To maintain ploidy through successive generations, meiosis must be followed by mitosis after the recovery of diploidy by fertilization. However, the coordination from meiotic to mitotic cycle is still unclear. Mos, the c-mos protooncogene product, is a key regulator of meiosis in vertebrates. In contrast to the previous observation that Mos functions only in vertebrate oocytes that arrest at meiotic metaphase II, here we isolate the first invertebrate mos from starfish and show that Mos functions also in starfish oocytes that arrest after the completion of meiosis II but not at metaphase II. In the absence of Mos, meiosis I is followed directly by repeated embryonic mitotic cycles, and its reinstatement restores meiosis II and subsequent cell cycle arrest. These observations imply that after meiosis I, oocytes have a competence to progress through the embryonic mitotic cycle, but that Mos diverts the cell cycle to execute meiosis II and remains to restrain the return to the mitotic cycle. We propose that a role of Mos that is conserved in invertebrate and vertebrate oocytes is not to support metaphase II arrest but to prevent the meiotic/mitotic conversion after meiosis I until fertilization, directing meiosis II to ensure the reduction of ploidy.

Footnotes

  • To whom reprint requests should be addressed. E-mail: tkishimo{at}bio.titech.ac.jp.

  • Data deposition: The sequence reported in this paper has been deposited in the GenBank database (accession no. AB040102).

  • Abbreviations:
    MEK,
    mitogen-activated protein kinase/extracellular signal-regulated kinase kinase;
    MAPKK,
    mitogen-activated protein kinase kinase;
    metaII,
    metaphase of meiosis II;
    1-MeAde,
    1-methyladenine;
    GST,
    glutathione S-transferase;
    GVBD,
    germinal vesicle breakdown
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