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

Commun Biol. 2022 Jan 11;5(1):30. doi: 10.1038/s42003-021-02956-8.

Abstract

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 PLCβ activity. On the other hand, the DAF-2c pathway promotes low-salt avoidance via PLCε and putative Akt phosphorylation sites on PLCε 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Avoidance Learning
  • Caenorhabditis elegans Proteins* / genetics
  • Caenorhabditis elegans Proteins* / metabolism
  • Caenorhabditis elegans* / genetics
  • Caenorhabditis elegans* / physiology
  • Insulin / genetics
  • Insulin / metabolism
  • Receptor, Insulin* / genetics
  • Receptor, Insulin* / metabolism
  • Signal Transduction / genetics
  • Sodium Chloride / metabolism
  • Starvation
  • Taste* / genetics
  • Taste* / physiology
  • Type C Phospholipases* / genetics
  • Type C Phospholipases* / metabolism

Substances

  • Caenorhabditis elegans Proteins
  • Insulin
  • ins-1 protein, C elegans
  • Sodium Chloride
  • Receptor, Insulin
  • Type C Phospholipases