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doi: 10.1242/10.1242/dev.00122
Department of Molecular, Cell, and Developmental Biology, Sinsheimer
Laboratories, University of California, Santa Cruz, CA 95064, USA
* Present address: Department of Biology, Queen's University, Kingston, Ontario
K7L 3N6, Canada
Author for correspondence (e-mail:
chisholm{at}biology.ucsc.edu)
Accepted 4 September 2002
The C. elegans genome encodes a single Eph receptor tyrosine kinase, VAB-1, which functions in neurons to control epidermal morphogenesis. Four members of the ephrin family of ligands for Eph receptors have been identified in C. elegans. Three ephrins (EFN-1/VAB-2, EFN-2 and EFN-3) have been previously shown to function in VAB-1 signaling. We show that mutations in the gene mab-26 affect the fourth C. elegans ephrin, EFN-4. We show that efn-4 also functions in embryonic morphogenesis, and that it is expressed in the developing nervous system. Interestingly, efn-4 mutations display synergistic interactions with mutations in the VAB-1 receptor and in the EFN-1 ephrin, indicating that EFN-4 may function independently of the VAB-1 Eph receptor in morphogenesis. Mutations in the LAR-like receptor tyrosine phosphatase PTP-3 and in the Semaphorin-2A homolog MAB-20 disrupt embryonic neural morphogenesis. efn-4 mutations synergize with ptp-3 mutations, but not with mab-20 mutations, suggesting that EFN-4 and Semaphorin signaling could function in a common pathway or in opposing pathways in C. elegans embryogenesis.
Key words: Morphogenesis, C. elegans, Ephrin, Semaphorin, EFN-4, VAB-1
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