View the Current Issue

Article

  • The EMBO Journal (2004) 23, 3984 - 3994
  • doi:10.1038/sj.emboj.7600417

Published online: 30 September 2004

PVR plays a critical role via JNK activation in thorax closure during Drosophila metamorphosis

Satoshi Ishimaru1, Ryu Ueda2,3, Yoshimi Hinohara4, Mayumi Ohtani1 and Hidesaburo Hanafusa1

  1. Laboratory of Molecular Oncology, Osaka Bioscience Institute, Furuedai, Suita, Osaka, Japan
  2. Genetic Strain Research Center, National Institute of Genetics, Mishima, Shizuoka, Japan
  3. Gene Function, Mitsubishi-Kagaku Institute of Life Sciences, Minami-ooya, Machida, Tokyo, Japan
  4. Fine Structure Analysis, Mitsubishi-Kagaku Institute of Life Sciences, Minami-ooya, Machida, Tokyo, Japan

Correspondence to:

Satoshi Ishimaru, Laboratory of Molecular Oncology, Osaka Bioscience Institute, 6-2-4 Furuedai, Suita, Osaka 565-0874, Japan. Tel.: +81 6 6872 4834; Fax: +81 6 6871 7521; E-mail: ishimas@obi.or.jp

Received 26 April 2004; Accepted 28 August 2004

PVR, the Drosophila homolog of the PDGF/VEGF receptor, has been implicated in border cell migration during oogenesis and hemocyte migration during embryogenesis. It was earlier shown that Mbc, a CDM family protein, and its effector, Rac, transduced the guidance signal from PVR during border cell migration. Here we demonstrate that PVR is also required for the morphogenetic process, thorax closure, during metamorphosis. The results of genetic and biochemical experiments indicate that PVR activates the JNK pathway. We present evidence showing Crk (an adaptor molecule), Mbc, ELMO (a homolog of Caenorhabditis elegans CED-12 and mammalian ELMO), and Rac to be mediators of JNK activation by PVR. In addition, we suppose that not only Rac but also Cdc42 is activated and involved in JNK activation downstream of PVR.

  • Keywords:

    • Crk–Mbc–ELMO complex,
    • JNK activation,
    • PVR,
    • Rac,
    • thorax closure