Dauer formation in C. elegans is modulated through AWC and ASI dependent chemosensation.

The perception of our surrounding environment is an amalgamation of stimuli detected by sensory neurons. In C. elegans olfaction is an essential behavior that determines various behavioral functions such as locomotion, feeding and development. Sensory olfactory cues also initiate downstream neuroendocrine signaling that controls ageing, learning, development and reproduction. Innate sensory preferences towards odors (food, pathogens) and reproductive pheromones are modulated by 11 pairs of amphid chemosensory neurons in the head region of C. elegans Amongst these sensory neurons, the ASI neuron has neuroendocrine functions and secretes neuropeptides, insulin-like peptide (DAF-28) and the TGF-β protein, DAF-7. Its expression levels are modulated by the presence of food (increased levels) and population density (decreased levels). A recent study has shown that EXP-1, an excitatory GABA receptor regulates DAF-7/TGF-β levels and participates in DAF-7/TGF- β mediated behaviors such as aggregation and bordering. Here, we show that exp-1 mutants show defective responses towards AWC sensed attractive odors in a non-autonomous manner through ASI neurons. Our dauer experiments reveal that in daf-7 mutants, ASI expressed EXP-1 and STR-2 (a G-protein coupled receptor) that partially maintained reproductive growth of animals. Further, studies suggest that neuronal connections between ASI and AWC neurons are allowed at least partially through ASI secreted DAF-7 or through alternate TGF- β pathway/s regulated by EXP-1 and STR-2. Together our behavioral, genetic and imaging experiments propose that EXP-1 and STR-2 integrate food cues and allow the animals to display DAF-7/TGF-β neuroendocrine dependent or independent behavioral responses contributing to chemosensensory and developmental plasticity.Significance statementThis work sheds light on a possible developmental and post-developmental function for the excitatory GABA receptor, EXP-1. We show that mutants of exp-1 are defective in their response towards AWC-sensed odors. Our genetic, behavioral and expression studies reveal that EXP-1 functions in the ASI neuron to modulate chemosensation and to regulate the behavioral switch between dauer and the reproductive state. EXP-1 has been shown to function in a DAF-7/TGF-β dependent manner. However, in the absence of DAF-7/TGF-β, EXP-1 and a G-protein coupled receptor, STR-2 integrate sensory information to maintain the reproductive state of the animal through an ASI dependent alternate pathway.