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  • The EMBO Journal (2002) 21, 4863 - 4874
  • doi:10.1093/emboj/cdf495

Fission yeast Mor2/Cps12, a protein similar to Drosophila Furry, is essential for cell morphogenesis and its mutation induces Wee1-dependent G2 delay

Dai Hirata1, Norihito Kishimoto1, Masako Suda1, Yuki Sogabe1, Sayuri Nakagawa1, Yasuko Yoshida1, Keisuke Sakai1, Masaki Mizunuma1, Tokichi Miyakawa1, Junpei Ishiguro2 and Takashi Toda3

  1. Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University, Higashi Hiroshima 739-8530, Japan
  2. Department of Biology, Faculty of Science and Engineering, Konan University, Okamoto 8-9-1, Kobe 658-8501, Japan
  3. Laboratory of Cell Regulation, Cancer Research UK, London Research Institute, PO Box 123, 44 Lincoln's Inn Fields, London WC2A 3PX, UK

Correspondence to:

Dai Hirata, E-mail: dhirata@hiroshima-u.ac.jp

Received 7 May 2002; Accepted 30 July 2002; Revised 22 July 2002

Fission yeast cells identify growing regions at the opposite ends of the cell, producing the rod-like shape. The positioning of the growth zone(s) and the polarized growth require CLIP170-like protein Tip1 and the Ndr kinase Orb6, respectively. Here, we show that the mor2/cps12 mutation disrupts the localization of F-actin at the cell ends, producing spherical cells and concomitantly inducing a G2 delay at 36°C. Mor2 is important for the localization of F-actin at the cell end(s) but not at the medial region, and is essential for the restriction of the growth zone(s) where Tip1 targets. Mor2 is homologous to the Drosophila Furry protein, which is required to maintain the integrity of cellular extensions, and is localized at both cell ends and the medial region of the cell in an actin-dependent fashion. Cellular localization of Mor2 and Orb6 was interdependent. The tyrosine kinase Wee1 is necessary for the G2 delay and maintenance of viability of the mor2 mutant. These results indicate that Mor2 plays an essential role in cell morphogenesis in concert with Orb6, and the mutation activates the mechanism coordinating morphogenesis with cell cycle progression.

  • Keywords:

    • actin,
    • checkpoint,
    • CLIP170,
    • Furry,
    • growth polarity