DAF-2c signaling promotes taste avoidance after starvation in Caenorhabditis elegans by controlling distinct phospholipase C isozymes

Previously, we reported that DAF-2c, an axonal insulin receptor isoform in Caenorhabditis elegans, acts in the ASER gustatory neuron to regulate taste avoidance learning, a process in which worms learn to avoid salt concentrations experienced during starvation. Here, we show that secretion of INS-1, an insulin-like peptide, after starvation conditioning is sufficient to drive taste avoidance via DAF-2c signaling. Starvation conditioning enhances the salt-triggered activity of AIA neurons, the main sites of INS-1 release, which potentially promotes feedback signaling to ASER to maintain DAF-2c activity during taste avoidance. Genetic studies suggest that DAF-2c-Akt signaling promotes high-salt avoidance via a decrease in PLC beta activity. On the other hand, the DAF-2c pathway promotes low-salt avoidance via PLC epsilon and putative Akt phosphorylation sites on PLC epsilon are essential for taste avoidance. Our findings imply that animals disperse from the location at which they experience starvation by controlling distinct PLC isozymes via DAF-2c. Masahiro Tomioka et al. study the function of a DAF-2c signaling pathway in salt avoidance after conditioning C. elegans with starvation. Their results suggest that taste avoidance behavior may depend on the control of distinct PLC isozymes via DAF-2c

Automated summary

This study investigates the function of the DAF-2c signaling pathway in salt avoidance after starvation conditioning in Caenorhabditis elegans. The results suggest that taste avoidance behavior may rely on the control of distinct PLC isozymes via DAF-2c.