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

• Published in: The Journal of neuroscience 2011-02, Vol.31 (8), p.3007-3015
• Main Authors: Shinkai, Yoichi, Yamamoto, Yuta, Fujiwara, Manabi, Tabata, Takashi, Murayama, Takashi, Hirotsu, Takaaki, Ikeda, Daisuke D, Tsunozaki, Makoto, Iino, Yuichi, Bargmann, Cornelia I, Katsura, Isao, Ishihara, Takeshi
• Format: Article
• Language: English
• Subjects: Animals; Behavior, Animal - physiology; Caenorhabditis elegans - cytology; Caenorhabditis elegans - enzymology; Caenorhabditis elegans - genetics; Caenorhabditis elegans - physiology; Caenorhabditis elegans Proteins - genetics; Caenorhabditis elegans Proteins - physiology; Choice Behavior - physiology; Guanylate Cyclase - genetics; Guanylate Cyclase - physiology; Interneurons - cytology; Interneurons - enzymology; Protein-Tyrosine Kinases - genetics; Protein-Tyrosine Kinases - physiology; Receptor Protein-Tyrosine Kinases - genetics; Receptor Protein-Tyrosine Kinases - physiology; Receptors, Guanylate Cyclase-Coupled - genetics; Receptors, Guanylate Cyclase-Coupled - physiology
• ISSN: 0270-6474; 1529-2401
• DOI: 10.1523/JNEUROSCI.4691-10.2011

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 Cu(2+), 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.