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

Satoshi Ishimaru1, Ryu Ueda, Yoshimi Hinohara

  • 1Laboratory of Molecular Oncology, Osaka Bioscience Institute, Furuedai, Suita, Osaka, Japan. ishimas@obi.or.jp

The EMBO Journal
|October 1, 2004
PubMed

Insights

PVR, a receptor, is crucial for thorax closure in Drosophila. It activates the JNK pathway via Crk, Mbc, ELMO, and Rac/Cdc42, impacting developmental processes.

Area of Science:

  • Developmental Biology
  • Cell Signaling
  • Molecular Genetics

Background:

  • PVR (Drosophila PDGF/VEGF receptor homolog) is known to regulate cell migration.
  • Mbc and Rac were previously identified as signal transducers for PVR in border cell migration.

Purpose of the Study:

  • To investigate the role of PVR in the morphogenetic process of thorax closure during Drosophila metamorphosis.
  • To elucidate the molecular mechanisms by which PVR regulates this process, particularly its involvement with the JNK pathway.

Main Methods:

  • Genetic experiments in Drosophila melanogaster.
  • Biochemical assays to analyze protein interactions and pathway activation.

Main Results:

  • PVR is essential for thorax closure, a developmental process during metamorphosis.
  • PVR activation leads to the activation of the JNK pathway.
  • Crk, Mbc, ELMO, and Rac are identified as mediators of PVR-induced JNK activation.
  • Evidence suggests both Rac and Cdc42 are activated downstream of PVR and involved in JNK activation.

Conclusions:

  • PVR plays a critical role in Drosophila metamorphosis, specifically in thorax closure.
  • The PVR signaling pathway involves Crk, Mbc, ELMO, Rac, and Cdc42, culminating in JNK pathway activation.
  • This study expands the known functions of PVR beyond cell migration to include developmental morphogenesis.

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