Developmental plasticity and the evolution of novelty: on novel genes, chromatin remodeling and developmental switch mechanisms. Event

Developmental (phenotypic) plasticity - a widespread phenomenon in animals and plants - has been suggested to facilitate phenotypic diversity and novelty, and recent studies start to provide insight into associated molecular mechanisms. The nematode Pristionchus pacificus is a laboratory model for comparative mechanistic biology and shows phenotypic plasticity in its feeding structures by developing teeth-like denticles of two different forms. One mouth-form allows bacterial feeding, whereas the other one permits predatory feeding on nematodes and fungi (Bento et al., 2010). We analyzed the feeding dimorphism in Pristionchus nematodes by integrating developmental genetics with functional tests in divergent populations and species. We identified a regulator of plasticity, eud-1, that acts in a developmental switch (Ragsdale et al., 2013). Mutations in eud-1 eliminate one mouth form, whereas over-expression of eud-1 fixes this form. EUD-1 is a sulfatase that acts dosage-dependently and is sufficient to control the sexual dimorphism and micro- and macroevolutionary variation of feeding forms. EUD-1 is epistatic to known signaling cascades and results from lineage-specific gene duplications. Follow up studies indicate that eud-1 is the primary locus of regulation of the mouth dimorphism with a dominant role of chromatin remodeling involving a novel regulatory mechanisms using antisense RNAs. Finally, we tested how the new predatory behavior is incorporated into an already existing nervous system. We show that P. pacificus employed a rewiring of the pharyngeal nervous system rather than the invention of novel cells during the transition from bacteriovorous to predatory feeding (Bumbarger et al., 2013).

Bento et al., Nature, 466, 494-497 (2010)

Bumbarger et al., Cell, 152, 109-119 (2013)

Ragsdale et al., Cell, 155, 922-933 (2013)