Animals can sense many kinds of stimuli by their sensory neurons. These sensory signals are integrated with other sensory information, humoral conditions, and memories, and bring a consequent response. How do animals integrate these multiple information and produce a single response? To elucidate neural mechanisms of these sensory processing, we are studying the behavioral regulation by experiences in C. elegans.In C. elegans, well-fed animals show attractive chemotaxis to NaCl. However, when animals are conditioned with NaCl for a few hours without food, their chemotaxis to NaCl is suppressed because of adaptation to NaCl. When animals are conditioned with NaCl in the presence of food, this suppression is not observed. Thus, chemotaxis to NaCl depends on experiences of both NaCl and food during conditioning. In the course of studying the chemotaxis-defective mutants, we found that
mpk-1 MAP kinase mutants (loss-of-function) show a behavioral defect in this paradigm.
mpk-1 mutant animals cultured on NGM plates (with food and NaCl) do not show chemotaxis to NaCl. However, when they were conditioned in the absence of NaCl,
mpk-1 mutants turned to show chemotaxis to NaCl as wild-type. Furthermore, when
mpk-1 mutant animals were conditioned with NaCl and food again for 6 hours after they have been conditioned without NaCl, their chemotaxis to NaCl was suppressed, although wild-type animals did not show this suppression in the same conditioning. These observations suggest that
mpk-1 mutants adapted to NaCl even in the presence of food. In addition, similar phenotypes can be observed in
let-60 Ras,
lin-45 MAPKKK, and
mek-2 MAPKK mutant animals, suggesting that Ras-MAPK signaling regulates the plasticity of chemotaxis to NaCl depending on the presence of food. Next, to identify neurons in which MPK-1 functions for this behavioral plasticity, we carried out neuron-type-specific expression experiments of
mpk-1 cDNA in
mpk-1 mutant and examined their chemotaxis to NaCl. As the result,
mpk-1 expression in a set of neurons driven by
odr-2 promoter, including AIZ, AIB, RIF, PVP, RIV interneurons and some sensory neurons, restored chemotaxis defect of a
mpk-1 mutant, although expression of MPK-1 in sensory neurons could not restore their defect. These results suggest that MPK-1 is required for this behavioral plasticity to function in a few interneurons.Our study will elucidate the role of MPK-1 MAP kinase in the sensory plasticity in C. elegans, and give us helpful information to understand general mechanisms for sensory processing.