Abstract
Information about nutrient availability is assessed via largely unknown mechanisms to drive developmental decisions, including the choice of Caenorhabditis elegans larvae to enter into the reproductive cycle or the dauer stage. In this study, we show that CMK-1 CaMKI regulates the dauer decision as a function of feeding state. CMK-1 acts cell-autonomously in the ASI, and non cell-autonomously in the AWC, sensory neurons to regulate expression of the growth promoting daf-7 TGF-β and daf-28 insulin-like peptide (ILP) genes, respectively. Feeding state regulates dynamic subcellular localization of CMK-1, and CMK-1-dependent expression of anti-dauer ILP genes, in AWC. A food-regulated balance between anti-dauer ILP signals from AWC and pro-dauer signals regulates neuroendocrine signaling and dauer entry; disruption of this balance in cmk-1 mutants drives inappropriate dauer formation under well-fed conditions. These results identify mechanisms by which nutrient information is integrated in a small neuronal network to modulate neuroendocrine signaling and developmental plasticity.
Highlights
Discrete alternate phenotypes arising from a single genotype in response to varying environmental cues is referred to as polyphenism (Michener, 1961; Mayr, 1963; Stearns, 1989)
Expression of the daf-7 TGF-b and daf-28 insulin-like peptide (ILP) genes are downregulated in well-fed cmk-1 mutants, and we find that CMK-1 acts cell-autonomously in the ASI sensory neurons, and non cell-autonomously in the AWC sensory neurons, to regulate the expression of daf-7 and daf-28, respectively
To verify that pheromone-induced dauer formation in wild-type animals is suppressed by bacterial food, we quantified dauers formed in the presence of pheromone and different concentrations of non-replicative as well as replicative bacteria
Summary
Discrete alternate phenotypes arising from a single genotype in response to varying environmental cues is referred to as polyphenism (Michener, 1961; Mayr, 1963; Stearns, 1989). In well-studied cases as in insects, it has been shown that animals integrate sensory cues during specific developmental stages to promote the expression of alternate phenotypic traits via regulation of endocrine and neuromodulatory signaling (Simpson et al, 2011; Watanabe et al, 2014). Environmental cues that trigger developmental plasticity include pheromones, temperature, mechanical stimuli, and food (Nijhout, 2003; Simpson et al, 2011). The extent and adaptive value of polyphenism has been extensively discussed (Pfennig et al, 2010; Moczek et al, 2011), the underlying molecular and neuronal mechanisms that allow animals to sense and integrate signals from food and feeding-state signals in the context of other cues to regulate phenotypic plasticity are not fully understood
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