Molecular aspects of the genetic switch regulating phenotypic plasticity of feeding structures in Pristionchus pacificus and its relevance for evolution

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Dokumentart: Dissertation
Date: 2016
Language: English
Faculty: 7 Mathematisch-Naturwissenschaftliche Fakultät
7 Mathematisch-Naturwissenschaftliche Fakultät
Department: Biologie
Advisor: Sommer, Ralf J. (Prof. Dr.)
Day of Oral Examination: 2016-06-09
DDC Classifikation: 500 - Natural sciences and mathematics
570 - Life sciences; biology
Keywords: Plastizität , Genetik , Entwicklungsbiologie , Fadenwürmer , Pristionchus pacificus
Other Keywords:
nuclear hormone receptor
mouth form
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Phenotypic plasticity is a facilitator of evolutionary novelty and diversity and therefore, has a major influence on evolution. Still, little is known about the underlying molecular mechanisms of plasticity. The nematode model organism Pristionchus pacificus possesses a plastic mouth dimorphism consisting of a eurystomatous and a stenostomatous mouth form, which characterize the adult worm. With its hermaphroditic mode of reproduction, P. pacificus is well suited for detailed genetic investigations, which provided major insight into the molecular mechanisms of plasticity in recent years. The formation of this plastic phenotype is not only affected by environmental cues, but also by the sexual identity and a maternal influence. Multiple eurystomatous-form defective (eud) mutants were isolated and characterized by a forward genetic approach. Two major genes regulating plasticity were identified and both of these haploinsufficient genes located on the X chromosome are major constituents of a genetic switch mechanism. The potentially catalytic active sulfatase eud-1 is a master regulator gene of the mouth form. Its dosage-dependant switch mechanism is reflected in the quantitative eud-1 expression in evolutionary diverged strains of P. pacificus. Indeed the eud-1 gene is not only linked to microevolutionary divergence, but also macroevolutionarily conserved in function, which was shown for its sister species Pristionchus exspectatus. The second switch gene is Ppa-nhr-40. The nuclear hormone receptor Ppa-nhr-40 acts downstream of eud-1 and completely reverts the all stenostomatous phenotype of eud-1 into an all eurystomatous phenotype. Together, this work shows that the development of phenotypic plasticity is regulated by a signaling network and is indeed genetically traceable. While genetic regulation and developmental switches have long been anticipated to control plasticity, this study is the first to contribute empirical evidence for their existence and to provide associated molecular mechanisms.

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