Multiple p38/JNK mitogen-activated protein kinase (MAPK) signaling pathways mediate salt chemotaxis learning in C. elegans

Animals are able to adapt their behaviors to the environment. In order to achieve this, the nervous system plays integrative roles, such as perception of external signals, sensory processing, and behavioral regulations via various signal transduction pathways. Here genetic analyses of Caenorhabditis elegans (C. elegans) found that mutants of components of JNK and p38 mitogen-activated protein kinase (MAPK) signaling pathways, also known as stress-activated protein kinase (SAPK) signaling pathways, exhibit various types of defects in the learning of salt chemotaxis. C. elegans homologs of JNK MAPKKK and MAPKK, and , respectively, are required for avoidance of salt concentrations experienced during starvation. In contrast, homologs of p38 MAPKKK and MAPKK, and , respectively, are required for high-salt chemotaxis after conditioning. Genetic interaction analyses suggest that a JNK family MAPK, , functions downstream of both signaling pathways to regulate salt chemotaxis learning. Furthermore, we found that the / pathway functions in sensory neurons, ASH, ADF, and ASER, to regulate the learned high-salt chemotaxis. A neuropeptide, , expressed in ASH, ADF, and ASER neurons, and a neuropeptide receptor, , expressed in AIA interneurons that receive synaptic input from these sensory neurons, function in the same genetic pathway as / signaling. These findings suggest that this MAPK pathway may affect neuropeptide signaling between sensory neurons and interneurons, thus promoting high-salt chemotaxis after conditioning.

Automated summary

Genetic analyses of C. elegans mutants reveal that the JNK and p38 signaling pathways play crucial roles in salt chemotaxis learning. These pathways may regulate neuropeptide signaling between sensory neurons and interneurons to promote high-salt chemotaxis after conditioning.