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Jeb signals through the Alk receptor tyrosine kinase to drive visceral muscle fusion

Author

Listed:
  • Camilla Englund

    (Umeå University)

  • Christina E. Lorén

    (Umeå University)

  • Caroline Grabbe

    (Umeå University)

  • Gaurav K. Varshney

    (Umeå University)

  • Fabienne Deleuil

    (Umeå University
    Umeå University)

  • Bengt Hallberg

    (Umeå University)

  • Ruth H. Palmer

    (Umeå University)

Abstract

The Drosophila melanogaster gene Anaplastic lymphoma kinase (Alk) is homologous to mammalian Alk, a member of the Alk/Ltk family of receptor tyrosine kinases (RTKs)1. We have previously shown that the Drosophila Alk RTK is crucial for visceral mesoderm development during early embryogenesis2. Notably, observed Alk visceral mesoderm defects are highly reminiscent of the phenotype reported for the secreted molecule Jelly belly (Jeb)3. Here we show that Drosophila Alk is the receptor for Jeb in the developing visceral mesoderm, and that Jeb binding stimulates an Alk-driven, extracellular signal-regulated kinase-mediated signalling pathway, which results in the expression of the downstream gene duf (also known as kirre)4,5—needed for muscle fusion. This new signal transduction pathway drives specification of the muscle founder cells, and the regulation of Duf expression by the Drosophila Alk RTK explains the visceral-mesoderm-specific muscle fusion defects observed in both Alk and jeb mutant animals.

Suggested Citation

  • Camilla Englund & Christina E. Lorén & Caroline Grabbe & Gaurav K. Varshney & Fabienne Deleuil & Bengt Hallberg & Ruth H. Palmer, 2003. "Jeb signals through the Alk receptor tyrosine kinase to drive visceral muscle fusion," Nature, Nature, vol. 425(6957), pages 512-516, October.
    • Handle: RePEc:nat:nature:v:425:y:2003:i:6957:d:10.1038_nature01950
    DOI: 10.1038/nature01950
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    Cited by:

    1. Jianan Zhang & Yuko Tsutsui & Hengyi Li & Tongqing Li & Yueyue Wang & Salma Laraki & Sofia Alarcon-Frias & Steven E. Stayrook & Daryl E. Klein, 2025. "Structural basis for the interaction between the Drosophila RTK Sevenless (dROS1) and the GPCR BOSS," Nature Communications, Nature, vol. 16(1), pages 1-12, December.

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