Abstract
Food and feeding-state dependent changes in chemoreceptor gene expression may allow Caenorhabditis elegans to modify their chemosensory behavior, but the mechanisms essential for these expression changes remain poorly characterized. We had previously shown that expression of a feeding state-dependent chemoreceptor gene, srh-234, in the ADL sensory neuron of C. elegans is regulated via the MEF-2 transcription factor. Here, we show that MEF-2 acts together with basic helix-loop-helix (bHLH) transcription factors to regulate srh-234 expression as a function of feeding state. We identify a cis-regulatory MEF2 binding site that is necessary and sufficient for the starvation-induced down regulation of srh-234 expression, while an E-box site known to bind bHLH factors is required to drive srh-234 expression in ADL. We show that HLH-2 (E/Daughterless), HLH-3 and HLH-4 (Achaete-scute homologs) act in ADL neurons to regulate srh-234 expression. We further demonstrate that the expression levels of srh-234 in ADL neurons are regulated remotely by MXL-3 (Max-like 3 homolog) and HLH-30 (TFEB ortholog) acting in the intestine, which is dependent on insulin signaling functioning specifically in ADL neurons. We also show that this intestine-to-neuron feeding-state regulation of srh-234 involves a subset of insulin-like peptides. These results combined suggest that chemoreceptor gene expression is regulated by both cell-autonomous and non-cell-autonomous transcriptional mechanisms mediated by MEF2 and bHLH factors, which may allow animals to fine-tune their chemosensory responses in response to changes in their feeding state.
Highlights
Animals modify their chemosensory behavior depending on their feeding-state, which allows them, for instance, to optimize their food-search strategy [1]
Plasticity in chemoreceptor gene expression may be a simple strategy by which an animal can modulate its chemosensory responses in changing external and internal state conditions
We showed that chemoreceptor gene expression in ADL neurons are regulated remotely by basic helix-loop-helix (bHLH) factors acting in the intestine through an insulin-mediated signaling pathway, implying a sensory neuron-gut interaction for modulating chemoreceptor gene expression as a function of feeding state
Summary
Animals modify their chemosensory behavior depending on their feeding-state, which allows them, for instance, to optimize their food-search strategy [1]. A simple strategy by which animals can rapidly alter their chemosensory behavior is by dynamically changing the gene expression levels of chemoreceptors localized in chemosensory neurons. This form of plasticity in chemoreceptor gene expression is observed across phyla [2,3,4,5,6,7], but how feeding state signals are translated into expression level changes of chemoreceptor genes is poorly understood. A systematic analysis of all srh chemoreceptor gene family promoters found that a bi-partite E-box motif was sufficient to direct expression in ADL sensory neurons [12], suggesting that the E-box and its cognate binding proteins the basic Helix-Loop-Helix (bHLH) transcription factors may have important roles in the regulation of ADL-expressed chemoreceptor genes
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