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First published online 30 June 2004
doi: 10.1242/dev.01242
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1 Department of Developmental Biology, Wenner-Gren Institute, Stockholm
University, S-106 96 Stockholm, Sweden
2 Department of Medical Nutrition, Karolinska Institute, Stockholm, Sweden
3 Department of Natural Sciences, Södertörns Högskola, S-141 04
Huddinge, Sweden
4 Umeå Centre for Molecular Pathogenesis, Umeå University, S-901 87,
Umeå, Sweden
* Author for correspondence (e-mail: christos{at}devbio.su.se)
Accepted 27 April 2004
EGF-receptor ligands act as chemoattractants for migrating epithelial cells during organogenesis and wound healing. We present evidence that Rhomboid 3/EGF signalling, which originates from the midline of the Drosophila ventral nerve cord, repels tracheal ganglionic branches and prevents them from crossing it. rho3 acts independently from the main midline repellent Slit, and originates from a different sub-population of midline cells: the VUM neurons. Expression of dominant-negative Egfr or Ras induces midline crosses, whereas activation of the Egfr or Ras in the leading cell of the ganglionic branch can induce premature turns away from the midline. This suggests that the level of Egfr intracellular signalling, rather than the asymmetric activation of the receptor on the cell surface, is an important determinant in ganglionic branch repulsion. We propose that Egfr activation provides a necessary switch for the interpretation of a yet unknown repellent function of the midline.
Key words: Drosophila, ru, Egfr, Epithelial migration, VNC midline
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