The genetics of phenotypic plasticity in nematode feeding structures

Abstract

Phenotypic plasticity has been proposed as an ecological and evolutionary concept. Ecologically, it can help study how genes and the environment interact to produce robust phenotypes. Evolutionarily, as a facilitator it might contribute to phenotypic novelty and diversification. However, the discussion of phenotypic plasticity remains contentious in parts due to the absence of model systems and rigorous genetic studies. Here, we summarize recent work on the nematode Pristionchus pacificus, which exhibits a feeding plasticity allowing predatory or bacteriovorous feeding. We show feeding plasticity to be controlled by developmental switch genes that are themselves under epigenetic control. Phylogenetic and comparative studies support phenotypic plasticity and its role as a facilitator of morphological novelty and diversity.

Keywords: Pristionchus pacificus; epigenetics; nuclear hormone receptors; phenotypic plasticity; switch genes.

Figure 1.

Pristionchus pacificus and growth. (a) Adult hermaphrodites lay eggs that develop through four larval stages to become adult. The first juvenile stage remains in the eggshell in P. pacificus. Under harsh and unfavourable conditions, worms develop into an arrested and long-lived dauer stage. (b) In the laboratory, worms are grown on agar plates with Escherichia coli as food source. Under these conditions, worms complete their direct life cycle in 4 days (20°). (c) The oriental beetle Exomala orientalis from Japan and the United States is one of the scarab beetle hosts on which P. pacificus is found in the dauer larval stage.

Figure 2.

Genetic regulation of phenotypic plasticity of P. pacificus feeding structures. (a) Mouth dimorphism. During larval development, P. pacificus individuals make an irreversible decision to develop a eurystomatous morph with two teeth (orange and black arrows) and a broad buccal cavity (white arrow), or alternatively, a stenostomatous morph with a single dorsal tooth (orange arrow) and a narrow buccal cavity (white arrow). (b) Under fixed laboratory conditions, mouth-form plasticity shows stochastic regulation resulting in hermaphrodites having approximately 70% eurystomatous mouth-forms, whereas males have been 10–30% eurystomatous animals. In genetic screens, monomorphic mutants can be isolated that are either 100% stenostomatous or 100% eurystomatous. (c) Partial genetic network regulating mouth-form plasticity. The sulfatase-encoding eud-1 gene and the nuclear hormone receptor are developmental switch mutations, which are dominant, loss-of-function and dosage dependent, resulting in all-stenostomatous or all-eurystomatous phenotypes, respectively. Small molecule signalling acts upstream of eud-1 and involves pheromones and steroid hormone signalling, which are not a subject of this review. Histone modifications are crucial for mouth-form regulation and act through an antisense message at the eud-1 locus (as-eud-1).