Many nematodes show a stage-specific behavior called nictation in which a worm stands on its tail and waves its head in three dimensions. Here we show that nictation is a dispersal behavior regulated by a specific set of neurons, the IL2 cells, in C. elegans. We established assays for nictation and showed that cholinergic transmission was required for nictation. Cell type-specific rescue experiments and genetic ablation experiments revealed that the IL2 ciliated head neurons were essential for nictation. Intact cilia in IL2 neurons, but not in other ciliated head neurons, were essential, as the restoration of the corresponding wild-type gene activity in IL2 neurons alone in cilia-defective mutants was sufficient to restore nictation. Optogenetic activation of IL2 neurons induced nictation, suggesting that signals from IL2 neurons are sufficient for nictation. Finally, we demonstrated that nictation is required for transmission of C. elegans to a new niche using flies as artificial carriers, suggesting a role of nictation as a dispersal and survival strategy under harsh conditions.
Bibliographical noteFunding Information:
This work was initiated when J.L. was at his sabbatical leave in M. Han’s laboratory (University of Colorado at Boulder). The authors thank Y. Kohara (National Institute of Genetics, Japan) for cDNA clones, A. Fire (Stanford University) for vectors, the J. Yim laboratory and the C.K. Chung laboratory (Seoul National University) for providing flies for our experiment, A. Gottschalk (Goethe University) for the ChR2 plasmid, P. Sengupta (Brandeis University) for the daf-10 cDNA plasmid and the Caenorhabditis Genetics Center for C. elegans strains. This work was supported by Brain Research Center of the 21st Century Frontier Research Program, the World Class University program and Research Center for Functional Cellulomics. M.C. was supported by Hi Seoul Science Fellowship from the Seoul Scholarship Foundation.
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