Feeding state either hunger or satiation can dramatically alter an animal's olfactory response to odors. Dynamic changes in the expression of chemoreceptor (CR) genes may underlie some of these changes in olfactory behavior. We have shown for the first time that CR gene expression in the olfactory neuron type, ADL, in C. elegans is modulated by feeding state. We found that the candidate chemoreceptor,
srh-234, in ADL is expressed when animals are fed, but not when animals are starved. Using subcellular laser surgery and genetic analysis, we showed that ADL likely functions cell-autonomously as a food sensor to regulate
srh-234 expression. However, when animals are fed inedible food that produces the same odor profile as edible food, the expression of
srh-234 was reduced. These results suggest that both food signals and internal nutritional signals regulate
srh-234 expression in ADL. What are the molecular and neural mechanisms underlying this plasticity in
srh-234 expression? Enhancing ADL output by expressing
pkc-1(gf) exclusively in ADL enhances the expression of
srh-234, whereas blocking ADL output by expressing tetanus toxin in ADL does not significantly affect
srh-234 expression. Thus, peptide signals secreted from ADL may modulate
srh-234 expression. We show that neuropeptide Y receptor,
npr-1, signaling in RMG interneurons connecting to ADL via gap junctions regulate
srh-234 gene expression in ADL. Modulation of CR gene expression is thought to be defined primarily by external inputs and not by circuit inputs. Our results reveal for the first time that, in addition to the cell-autonomous function of ADL, feedback modulation from RMG regulates CR gene expression in ADL. We propose an intriguing model by which feeding state- and NPR-1-dependent regulation of CR genes alter sensory perception in ADL. We expect that our findings will not only yield insights into the mechanisms underlying CR expression in sensory neurons in other organisms, but also provide information regarding the basic mechanisms underlying olfactory plasticity.