CGC Bibliography Paper 5631

The divergent C. elegans ephrin EFN-4 functions in embryonic morphogenesis in a pathway independent of the VAB-1 Eph receptor.

Chin-Sang ID, Moseley SL, Ding M, Harrington RJ, George SE, Chisholm AD

Medline:
12403719
Citation:
Development 129: 5499-5510 2002
Type:
ARTICLE
Genes:
efn-1 efn-2 efn-3 efn-4 mab-20 mab-26 ptp-3 vab-1 vab-2
Abstract:
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