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.
Highlights
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
In Caenorhabditis elegans, an Insulin-like peptides (ILPs), INS-1, acts on an insulin receptor homolog, DAF-2, and its downstream PI 3-kinase (PI3K)–Akt signaling in the ASER gustatory neuron, the rightsided ASE class of amphid sensory neurons, to regulate taste avoidance learning, a process in which worms learn to avoid salt concentrations experienced during starvation[9,10]
We have reported that worms with a large deletion mutation of ins-1, namely ins-1(nr2091)[29], were attracted to salt concentrations experienced during feeding similar to the wild type (Supplementary Fig. 1); they showed significant defects in both low- and high-salt migration after high- and low-salt conditioning in the absence of food, respectively (Fig. 1a, b)25. daf-2c(pe2722) mutants, which harbor a frameshift deletion in the cassette exon 11.5, and daf-16(mgDf50) mutants, which harbor a large deletion in a daf-16 locus, show significant defects in taste avoidance learning (Fig. 1b)[12]
Summary
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. In Caenorhabditis elegans, an ILP, INS-1, acts on an insulin receptor homolog, DAF-2, and its downstream PI 3-kinase (PI3K)–Akt signaling in the ASER gustatory neuron, the rightsided ASE class of amphid sensory neurons, to regulate taste avoidance learning, a process in which worms learn to avoid salt concentrations experienced during starvation[9,10]. Correlations exist between DAG dynamics and migration direction in salt chemotaxis of worms after feeding: DAG levels at the ASER axon are increased by a decrease in ambient salt concentration, whereby well-fed worms migrate toward high salt concentrations; in contrast, DAG levels are decreased by an increase in ambient salt concentration, thereby leading worms to move toward low salt concentrations This mechanism allows worms to remain in the location at which they were fed[26]. C. elegans PLC-1 harbors the domains required for binding such GTPases[28], it is unclear how PLC-1 activity is regulated
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