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Abstract

Developmental plasticity has been suggested to facilitate the evolution of novelty and phenotypic diversity, but molecular mechanisms underlying this relationship are little understood. The nematode Pristionchus pacificus is a model system for integrative evolutionary biology, combining laboratory studies with field work in ecology and population genetics. Pristionchus pacificus shows phenotypic plasticity in its feeding structures and is able to feed on fungi and other nematodes. Pristionchus executes one of two alternative mouth- forms (Eurystomatous vs. Stenostomatous) after an irreversible developmental decision that requires small molecule pheromones consisting of a blend of ascarosides and paratosides. Interestingly, dauer formation and mouth-form regulation require novel and specific compounds for their regulation. Downstream of small molecule pheromones and a conserved endocrine signaling module involving the nuclear hormone receptor DAF-12, we identified a novel regulator of plasticity eud-1. eud-1 acts in a developmental switch; eud-1 mutations eliminate one mouth form, whereas over-expression of eud- 1 fixes it. EUD-1 is a sulfatase that acts dosage- dependently, is necessary and sufficient to control the sexual dimorphism of feeding forms, and has a conserved function in Pristionchus evolution. eud- 1 represents a novel gene that is much younger than the feeding dimorphism and has been added to a complex genetic network at a terminal position. It is epigenetically regulated in part by genes that are not conserved. These studies show that novel structures are determined by an unpredictable mix of conserved (co-opted) and novel determinants and that candidate gene approaches are of limited use for studying novel biological phenomena.