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Unformatted text preview: INTRODUCTION The epidermis of C. elegans is a simple epithelium that forms the skin of the animal. Morphogenesis of the C. elegans epidermis provides a model for several aspects of epithelial biology, including epithelial cell fate determination, cell polarity, cell motility and cell shape (Chin-Sang and Chisholm, 2000; Michaux et al., 2001; Simske and Hardin, 2001). Epidermal cells arise on the dorsal surface of the embryo, where they form junctions to give rise to an epithelial sheet. The epidermal sheet then spreads laterally and ventrally to close up at the ventral midline, an example of epiboly referred to in C. elegans as epidermal enclosure (Williams-Masson et al., 1997). Epidermal enclosure itself can be divided into two steps: in the first step, two bilateral pairs of epidermal cells extend actin-rich processes over a substrate of neural cells. These processes meet their contralateral counterparts at the ventral midline, leading to the rapid formation of junctions between the two pairs of cells (Raich et al., 1999). In the second step, other epidermal cells enclose the posterior body, possibly by a supracellular actin purse-string mechanism (Simske and Hardin, 2001). We have previously shown that the C. elegans Eph receptor VAB-1 and its ephrin ligand EFN-1 (previously called VAB-2) function in epidermal enclosure (Chin-Sang et al., 1999; George et al., 1998). During epidermal enclosure, VAB-1 and EFN-1 are predominantly expressed and required in underlying neurons but not in the epidermal cells. Time-lapse analysis of vab-1 and efn-1 mutant embryos revealed specific defects in the organization of neural precursors, manifested as a failure to close the gastrulation cleft, a depression in the ventral surface of the embryo left after ingression of endodermal and mesodermal precursors. Because epidermal cells migrate over the descendants of these ventral neural precursors, a simple model for the non-autonomous effects of vab-1 or ephrin mutants on epidermal enclosure is that they arise as a consequence of an altered neural substrate. The defects in neural cell organization in C. elegans Eph signaling mutants may resemble cell sorting defects observed in vertebrates when Eph signaling is disrupted (Mellitzer et al., 1999; Xu et al., 2000). The relative simplicity of the C. elegans Eph signaling network allows a systematic analysis of its roles in a single morphogenetic process. A single Eph receptor (VAB-1) and four ephrins (EFN-1 through EFN-4) have been identified in C. elegans (Wang et al., 1999). efn-1 mutations, obtained from forward genetic screens, cause phenotypes weaker than but otherwise indistinguishable from those of vab-1 mutants; 5499 Development 129, 5499-5510 2002 The Company of Biologists Ltd doi:10.1242/dev.00122 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...
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This note was uploaded on 12/06/2011 for the course BIOL 430 taught by Professor Dr.ianchin-sang during the Winter '10 term at Queens University.
- Winter '10