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Cell. 2013 Nov 7;155(4):922-33. doi: 10.1016/j.cell.2013.09.054.

A developmental switch coupled to the evolution of plasticity acts through a sulfatase.

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Department of Evolutionary Biology, Max Planck Institute for Developmental Biology, 72076 Tübingen, Germany.


Developmental plasticity has been suggested to facilitate phenotypic diversity, but the molecular mechanisms underlying this relationship are little understood. We analyzed a feeding dimorphism in Pristionchus nematodes whereby one of two alternative adult mouth forms is executed after an irreversible developmental decision. By integrating developmental genetics with functional tests in phenotypically divergent populations and species, we identified a regulator of plasticity, eud-1, that acts in a developmental switch. eud-1 mutations eliminate one mouth form, whereas overexpression 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. It is epistatic to known signaling cascades and results from lineage-specific gene duplications. EUD-1 thus executes a developmental switch for morphological plasticity in the adult stage, showing that regulatory pathways can evolve by terminal addition of new genes.

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