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Abstract

The nematode Pristionchus pacificus has been established as a “satellite model organism” in evolutionary developmental biology and is compared to Caenorhabditis elegans. P. pacificus allows comparative forward and reverse genetic studies at the level of homologous cells. Formation of the vulva, the egg-laying apparatus of the worm, provides a paradigm to study the evolution of signaling processes. Both nematodes form their vulvae from three vulval precursor cells (VPCs). C. elegans has a total of six VPCs competent to form the vulva, in contrast in P. pacificus only those three cells that will form the vulva are actually competent to respond to inductive signaling. The P. pacificus VEG is reduced in cell number with respect to C. elegans because of the programmed cell death (PCD) of two anterior cells, P3.p and P4.p, and the specialized cell fate of P8.p. We have used a forward genetic approach to study the regulatory mechanisms of VEG evolution. Two complementation groups, ped-5 and ped-6, specifically regulate the programmed cell death of P3.p and P4.p. and were shown to encode homologs of Drosophila Hairy and Groucho. We have shown that Hairy/Groucho act by regulating the HOX gene lin-39, which specifies the VEG (Schlager et al., 2006). More recently we have isolated mutants that change the specialized cell fate of the posterior cell P8.p. One of these mutants represents a novel multivulva phenotype unknown from C. elegans or previously known mutants in P. pacificus. We will describe the molecular network regulating P. pacificus vulva formation and will provide insight into the evolutionary modifications of developmental processes, as exemplified by the nematode vulva.