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          Institute: MPI für Entwicklungsbiologie     Collection: Abteilung 4 - Evolutionary Biology (R. Sommer)     Display Documents

ID: 733059.0, MPI für Entwicklungsbiologie / Abteilung 4 - Evolutionary Biology (R. Sommer)
The Nuclear Hormone Receptor NHR-40 Acts Downstream of the Sulfatase EUD-1 as Part of a Developmental Plasticity Switch in Pristionchus
Authors:Kieninger, M. R.; Ivers, N. A.; Rodelsperger, C.; Markov, G. V.; Sommer, R. J.; Ragsdale, E. J.
Date of Publication (YYYY-MM-DD):2016-08-22
Title of Journal:Curr Biol
Issue / Number:16
Start Page:2174
End Page:2179
Review Status:Internal review
Audience:Not Specified
Abstract / Description: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.
External Publication Status:published
Document Type:Article
Communicated by:MPI für Entwickungsbiologie
Affiliations:MPI für Entwicklungsbiologie/Abteilung 4 - Evolutionsbiologie (Ralf J. Sommer)
External Affiliations:Department of Biology, Indiana University, 915 East Third Street, Bloomington, IN 47405, USA. Department of Evolutionary Biology, Max Planck Institute for Developmental Biology, 72076 Tubingen, Germany; Sorbonne Universites, UPMC University of Paris 06, CNRS, UMR 8227 Integrative Biology of Marine Models, Station Biologique de Roscoff, CS 90074, 29688 Roscoff Cedex, France. Department of Biology, Indiana University, 915 East Third Street, Bloomington, IN 47405, USA. Electronic address:
Identifiers:ISSN:1879-0445 (Electronic) 0960-9822 (Linking) %R 10.1... [ID No:1]
URL: [ID No:2]
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