The C. elegans vulva provides a simple model for the genetic analysis of pattern formation and organ morphogenesis during metazoan development. During specification three ventral hypodermal cells are induced to form the vulva, and during morphogenesis the planar array of their twenty-two descendents is transformed by shape changes, migrations and cell fusions into a stack of seven syncytial toroid-shaped cells (vulA-vulF) that surround a lumen (Sharma-Kishore et al., Dev. 126: 691, Wang and Sternberg, Curr. Top. Dev. Biol. 51: 189). The par (cytoplasmic partition defective) genes play essential roles in establishing polarity in the early embryo, but because of their maternal effect genetics, have been thought to play little role outside of the early embryo. We have previously shown that postembryonic RNAi of
par-1 causes a protruding vulva phenotype that is likely the result of specific defects during vulval morphogenesis (Hurd and Kemphues, Dev. Biol. 253: 54). This observation raised the question of what if any role the other par genes play during vulval development. Given that components of the PAR-3/PAR-6/PKC-3/CDC-42 (anterior/apical) signaling complex are expressed in the vulva (Hurd and Kemphues, Dev. Biol. 253: 54) we asked whether post-embryonic depletion of these proteins or of NMY-2, a myosin shown to bind to PAR-1 (Guo and Kemphues, Nature 382: 455) caused defects in vulval development. We found that RNAi depletion of CDC-42, NMY-2 or PKC-3 caused moderate to low penetrance Pvl among other postembryonic phenotypes. We have used an AJM-1::GFP and an HMP-1::GFP strain to further characterize the cellular and developmental defects that underlie these Pvl phenotypes and our preliminary results suggest that depletion of CDC-42, which causes the highest Pvl penetrance, seems to cause defects in both specification and morphogenesis. These results suggest that signalling through the apical complex might play multiple roles during the development of the vulva.