C. elegans responds to water-soluble chemicals such as ions and amino acids, and senses acid pH (H+) and alkaline pH (OH-) as nociceptive and attractive stimuli, respectively (Ward, 1973; Dusenbery, 1974). Sambongi et al. (2000) have shown some of C. elegans amphid chemosensory neurons are responsible for acid pH avoidance by ablating these neurons. However, neuronal networks involved in the pH responses still remain to be explored not only in C. elegans but also in any animals. We have developed an assay system to study C. elegans response behaviors to alkaline pH. On an assay plate with a pH gradient from pH 7.0 to pH 9.5, wild-type animals were attracted toward alkaline pH along the gradient. When behaviors of some chemotaxis defective mutants were analyzed, furthermore, che-1
were found to avoid higher pH regions on the assay plate. Because che-1
is deficient in differentiation of ASE chemosensory neurons, the result suggests that ASE is required for chemotaxis toward alkaline pH, and some other neurons are responsible for higher alkaline pH avoidance. Furthermore, ASE-specific DYF-3 expression in dyf-3
mutants defective in gustatory chemosensation could rescue the worms to be attracted toward alkaline pH. These results indicate that ASE functions are necessary and sufficient for the chemotaxis toward alkaline pH. On assay plates with a pH gradient from pH 7.0 to pH 11.0, wild type animals avoided pH higher than pH10.0. This suggests that C. elegans has neurons for alkaline avoidance. Along the pH gradient, ASE-rescued dyf-3
was attracted beyond pH 10.0, suggesting that ASE neurons function only for chemoattraction to alkaline pH. As described above, daf-6
avoided higher pH regions. As daf- 6 mutants are defective in sensory pore formation for amphid and phasmid neurons, but have normal structure in IL2 chemosensory endings (Albert et al., 1981), the result implies that IL2 chemosensory neurons may be involved in the alkaline pH avoidance. Neuronal networks responsible for the alkaline pH attraction and avoidance will also be discussed. Ward (1973), PNAS 70, 817. Dusenbery (1974), J. Exp. Zool. 188, 41. Sambongi et al. (2000), Neuroreport 11, 2229. Albert et al. (1981), J. Comp. Neurol. 198, 435.