Mechanisms of Feeding State Dependent Chemoreceptor Gene Expression in C. elegans

Abstract

Animals dramatically modify their chemosensory behaviors when starved, which could allow them to alter and optimize their food-search strategies. Dynamic changes in the gene expression of chemoreceptors may be a general mechanism underlying food and state-dependent changes in chemosensory behaviors. In our recent studies [1,2], we identified chemoreceptors in the ADL sensory neuron type of C. elegans that are modulated by feeding state and food availability. Here, we highlight our recent findings by which sensory inputs into ADL, neuropeptide secretion from ADL, gap junction inputs from the RMG interneuron, and neuroendocrine signaling between the intestine and ADL, are required to regulate an ADL-expressed chemoreceptor. This sensory and circuit-mediated regulation of chemoreceptor gene expression is dependent on cell-autonomous pathways acting in ADL, including MEF-2, a network of basic helix-loop-helix (bHLH) transcription factors, DAF-2, OCR-2 and calcium signaling, and circuit inputs from RMG mediated by NPR-1. Based on these findings, we propose an intriguing but speculative feedback modulatory circuit mechanism by which sensory perception of food and neuroendocrine signaling are coupled to regulate ADL-expressed chemoreceptors, which may allow animals to precisely regulate and fine-tune their chemosensory neuron responses as a function of feeding state.