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First published online 20 July 2005
doi: 10.1242/dev.01947
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Department of Biology, Queen's University, Kingston, Ontario K7L 3N6, Canada
* Author for correspondence (e-mail: chinsang{at}biology.queensu.ca)
Accepted 20 June 2005
Mutations that affect the single C. elegans Eph receptor tyrosine kinase VAB-1 cause defects in cell movements during embryogenesis. Here, we provide genetic and molecular evidence that the VAB-1 Eph receptor functions with another neuronal receptor, SAX-3/Robo, for proper embryogenesis. Our analysis of sax-3 mutants shows that SAX-3/Robo functions with the VAB-1 Eph receptor for gastrulation cleft closure and ventral epidermal enclosure. In addition, SAX-3 functions autonomously for epidermal morphogenesis independently of VAB-1. A double-mutant combination between vab-1 and slt-1 unmasks a role for the SLT-1 ligand in embryogenesis. We provide evidence for a physical interaction between the VAB-1 tyrosine kinase domain and the juxtamembrane and CC1 region of the SAX-3/Robo receptor. Gene dosage, non-allelic non-complementation experiments and co-localization of the two receptors are consistent with a model in which these two receptors form a complex and function together during embryogenesis.
Key words: Eph Receptor Tyrosine Kinase, Robo receptor, Morphogenesis, Cell movements, C. elegans, Synthetic lethal
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