C. elegans can memorize environmental temperatures and migrate toward the cultivation temperature when they are placed on a thermal gradient. This behavior, called thermotaxis, provides an ideal model system to study neural mechanisms by which animals express behavior, since a simple neural circuit required for this behavior is identified previously (Mori & Ohshima, 1995). To investigate mechanisms that underlie thermotaxis, we previously performed genetic screens and isolated
nj24 (Mohri et al., 2005). Further characterization of the mutant in this study revealed an interesting thermotaxis phenotype, in which
nj24 migrates "slightly" higher temperature than its cultivation temperature, implying the existence of elaborate and delicate mechanisms that regulate thermotaxis. Genetic mapping of
nj24 revealed that
nj24 is a mutant for the
inx-4 gene, which encodes a member of innexins that are thought to constitute gap junctions in C. elegans. To identify cells expressing INX-4, we observed the expression pattern of
inx-4::gfp and found that INX-4 is expressed in the nervous system, including some neurons that are known to be important for thermotaxis (AFD, AWC, AIY, RIA). Cell-specific rescue experiments revealed that expressing INX-4 in AFD thermosensory neurons is sufficient to rescue the abnormal thermophilic phenotype of
inx-4 mutants, suggesting that INX-4 in AFD is required to regulate thermotaxis behavior. Interestingly, while conducting AFD-specific rescue experiment, we introduced three different doses of
inx-4 cDNA into AFD and found that higher dose causes strong cryophilic phenotype, implicating a possibility that the expression level of INX-4 in AFD is crucial to determine behavioral outputs. Our study showed that the innexin function in C. elegans major sensory neurons is important to regulate thermotaxis behavior. We believe that further analysis will elucidate fundamental functions of innexin, gap junction component, in the nervous system to control behaviors.