title: The Nuclear Hormone Receptor NHR-40 Acts Downstream of the Sulfatase EUD-1 as Part of a Developmental Plasticity Switch in Pristionchus.
abstract: Developmental plasticity, the ability of one genotype to produce distinct phenotypes in different environments, has been suggested to facilitate phenotypic diversification, and several examples in plants and animals support its macroevolutionary potential [1-8]. However, little is known about associated molecular mechanisms, because environmental effects on development are difficult to study by laboratory approaches. One promising system is the mouth dimorphism of the nematode Pristionchus pacificus [9-12]. Following an irreversible decision in larval development, these nematodes form moveable teeth that occur in either of two discrete morphs. The "eurystomatous" (Eu) form has a wide mouth and two teeth, allowing predatory feeding on other nematodes. In contrast, the alternative ("stenostomatous"; St) form has diminutive mouthparts that largely constrain its diet to microbes. The sulfatase EUD-1 was previously discovered to execute a polyphenism switch based on dosage of functional alleles [13] and confirmed a prediction of evolutionary theory about how developmental switches control plasticity [1, 3]. However, the genetic context of this single gene, and hence the molecular complexity of switch mechanisms, was previously unknown. Here we use a suppressor screen to identify factors downstream of eud-1 in mouth-form regulation. We isolated three dominant, X-linked mutants in the nuclear hormone receptor gene nhr-40 that are haploinsufficient. Both eud-1 nhr-40 double and nhr-40 single mutants are all Eu, whereas transgenic overexpression of nhr-40 does not restore the wild-type phenotype but instead results in nearly all-St lines. Thus, NHR-40 is part of a developmental switch, suggesting that switch mechanisms controlling plasticity consist of multi-component hormonal signaling systems.
authors.affiliation: Department of Evolutionary Biology, Max Planck Institute for Developmental Biology, 72076 Tübingen, Germany.
authors.forename: Manuela R
authors.initials: MR
authors.lastname: Kieninger
authors.affiliation: Department of Biology, Indiana University, 915 East Third Street, Bloomington, IN 47405, USA.
authors.forename: Nicholas A
authors.initials: NA
authors.lastname: Ivers
authors.affiliation: Department of Evolutionary Biology, Max Planck Institute for Developmental Biology, 72076 Tübingen, Germany.
authors.forename: Christian
authors.initials: C
authors.lastname: Rödelsperger
authors.affiliation: Department of Evolutionary Biology, Max Planck Institute for Developmental Biology, 72076 Tübingen, Germany; Sorbonne Universités, UPMC University of Paris 06, CNRS, UMR 8227 Integrative Biology of Marine Models, Station Biologique de Roscoff, CS 90074, 29688 Roscoff Cedex, France.
authors.forename: Gabriel V
authors.initials: GV
authors.lastname: Markov
authors.affiliation: Department of Evolutionary Biology, Max Planck Institute for Developmental Biology, 72076 Tübingen, Germany.
authors.forename: Ralf J
authors.initials: RJ
authors.lastname: Sommer
authors.affiliation: Department of Biology, Indiana University, 915 East Third Street, Bloomington, IN 47405, USA. Electronic address: ragsdale@indiana.edu.
authors.forename: Erik J
authors.initials: EJ
authors.lastname: Ragsdale
mesh_terms: D000818:Animals; D018507:Gene Expression Regulation, Developmental; D057850:Hermaphroditic Organisms / Q000235:genetics / Q000254:growth & development; D007814:Larva / Q000033:anatomy & histology / Q000235:genetics / Q000254:growth & development; D008297:Male; D009055:Mouth / Q000033:anatomy & histology; D010641:Phenotype; D018160:Receptors, Cytoplasmic and Nuclear / Q000235:genetics* / Q000378:metabolism; D017168:Rhabditida / Q000033:anatomy & histology / Q000235:genetics* / Q000254:growth & development; D013429:Sulfatases / Q000235:genetics* / Q000378:metabolism; D014070:Tooth / Q000033:anatomy & histology
chemical_list: D018160:Receptors, Cytoplasmic and Nuclear; D013429:Sulfatases