Behavioral Choice between Conflicting Alternatives Is Regulated by a Receptor Guanylyl Cyclase, GCY-28, and a Receptor Tyrosine Kinase, SCD-2, in AIA Interneurons of Caenorhabditis elegans
- Yoichi Shinkai1,
- Yuta Yamamoto1,
- Manabi Fujiwara1,
- Takashi Tabata1,
- Takashi Murayama1,
- Takaaki Hirotsu1,
- Daisuke D. Ikeda2,
- Makoto Tsunozaki3,
- Yuichi Iino2,
- Cornelia I. Bargmann3,
- Isao Katsura4, and
- Takeshi Ishihara1,4
- 1Department of Biology, Graduate School of Sciences, Kyushu University, Fukuoka 812-8581, Japan,
- 2Department of Biophysics and Biochemistry, Graduate School of Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan,
- 3Howard Hughes Medical Institute, Laboratory of Neural Circuits and Behavior, The Rockefeller University, New York, New York 10065, and
- 4Structural Biology Center, National Institute of Genetics, Mishima 411-8540, Japan
- Correspondence should be addressed to Takeshi Ishihara, Department of Biology, Graduate School of Sciences, Kyushu University, Hakozaki 6-10-1, Higashi-ku, Fukuoka 812-8581, Japan, takeiscb{at}kyushu-u.org
Abstract
Animals facing conflicting sensory cues make a behavioral choice between competing alternatives through integration of the sensory cues. Here, we performed a genetic screen to identify genes important for the sensory integration of two conflicting cues, the attractive odorant diacetyl and the aversive stimulus Cu2+, and found that the membrane-bound guanylyl cyclase GCY-28 and the receptor tyrosine kinase SCD-2 regulate the behavioral choice between these alternatives in Caenorhabditis elegans. The gcy-28 mutants and scd-2 mutants show an abnormal bias in the behavioral choice between the cues, although their responses to each individual cue are similar to those in wild-type animals. Mutants in a gene encoding a cyclic nucleotide gated ion channel, cng-1, also exhibit the defect in sensory integration. Molecular genetic analyses suggested that GCY-28 and SCD-2 regulate sensory integration in AIA interneurons, where the conflicting sensory cues may converge. Genetic ablation or hyperpolarization of AIA interneurons showed nearly the same phenotype as gcy-28 or scd-2 mutants in the sensory integration, although this did not affect the sensory response to each individual cue. In gcy-28 or scd-2 mutants, activation of AIA interneurons is sufficient to restore normal sensory integration. These results suggest that the activity of AIA interneurons regulates the behavioral choice between the alternatives. We propose that GCY-28 and SCD-2 regulate sensory integration by modulating the activity of AIA interneurons.
- Copyright © 2011 the authors 0270-6474/11/313007-09$15.00/0





