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Abstract:
Environment shapes development through a phenomenon called developmental plasticity. Deciphering its genetic basis has potential to shed light on the origin of novel traits and adaptation to environmental change. However, molecular studies are scarce, and little is known about molecular mechanisms associated with plasticity. We investigated the gene regulatory network controlling predatory vs. non-predatory dimorphism in the nematode Pristionchus pacificus and found that it consists of genes of extremely different age classes. We isolated mutants in the conserved nuclear hormone receptor nhr-1 with previously unseen phenotypic effects. They disrupt mouth-form determination and result in animals combining features of both wild-type morphs. In contrast, mutants in another conserved nuclear hormone receptor nhr-40 display altered morph ratios, but no intermediate morphology. Despite divergent modes of control, NHR-1 and NHR-40 share transcriptional targets, which encode extracellular proteins that have no orthologs in Caenorhabditis elegans and result from lineage-specific expansions. An array of transcriptional reporters revealed co-expression of all tested targets in the same pharyngeal gland cell. Major morphological changes in this gland cell accompanied the evolution of teeth and predation, linking rapid gene turnover with morphological innovations. Thus, the origin of feeding plasticity involved novelty at the level of genes, cells and behavior.
Abstract:
Author summary:
Rather than following a pre-determined genetic “blueprint”, organisms can adjust their development when they perceive relevant environmental signals–a phenomenon called plasticity. This improves performance in changing environment and may also affect how species evolve. To learn how plasticity works on the mechanistic genetic level, we investigated the roundworm Pristionchus pacificus. It may develop either as a toothed predator or as a narrow-mouthed microbe-eater depending on food source and population density, an ability that evolved less than 100 million years ago. Previous studies identified switch genes, whose inactivation or overactivation forces either predatory or non-predatory development. Here, we identified the first core gene, which is required for the specification of both morphologies. It encodes a transcription factor, whose inactivation creates animals that appear intermediate between predators and non-predators. We queried which genes are simultaneously controlled by this previously unknown regulator and by a closely related protein that acts as a classical switch. All of the co-regulated genes were recently born and are acting in a single cell that was strongly modified when predator vs. non-predator plasticity evolved. We suggest that conserved regulators of different classes enlisted novel genes in a refurbished cell to regulate a novel plastic trait.
