Abstract
The nematode Caenorhabditis elegans learns the concentration of NaCl and moves toward the previously experienced concentration. In this behavior, the history of NaCl concentration change is reflected in the level of diacylglycerol and the activity of protein kinase C, PKC-1, in the gustatory sensory neuron ASER and determines the direction of migration. Here, through a genetic screen, we found that the activation of Gq protein compensates for the behavioral defect of the loss-of-function mutant of pkc-1 We found that Gq activation results in hyperproduction of diacylglycerol in ASER sensory neuron, which leads to recruitment of TPA-1, an nPKC isotype closely related to PKC-1. Unlike the pkc-1 mutants, loss of tpa-1 did not obviously affect migration directions in the conventional learning assay. This difference was suggested to be due to cooperative functions of the C1 and C2-like domains of the nPKC isotypes. Furthermore, we investigated how the compensatory capability of tpa-1 contributes to learning and found that learning was less robust in the context of cognitive decline or environmental perturbation in tpa-1 mutants. These results highlight how two nPKC isotypes contribute to the learning system.