Neuroendocrine modulation sustains the C. elegans forward motor state
Abstract
Neuromodulators shape neural circuit dynamics. Combining electron microscopy, genetics, transcriptome profiling, calcium imaging, and optogenetics, we discovered a peptidergic neuron that modulates C. elegans motor circuit dynamics. The Six/SO-family homeobox transcription factor UNC-39 governs lineage-specific neurogenesis to give rise to a neuron RID. RID bears the anatomic hallmarks of a specialized endocrine neuron: it harbors near-exclusive dense core vesicles that cluster periodically along the axon, and expresses multiple neuropeptides, including the FMRF-amide-related FLP-14. RID activity increases during forward movement. Ablating RID reduces the sustainability of forward movement, a phenotype partially recapitulated by removing FLP-14. Optogenetic depolarization of RID prolongs forward movement, an effect reduced in the absence of FLP-14. Together, these results establish the role of a neuroendocrine cell RID in sustaining a specific behavioral state in C. elegans.
Article and author information
Author details
Funding
Canadian Institutes of Health Research (CIHR MOP to Mei Zhen)
- Mei Zhen
National Institutes of Health (NIH award to John Calarco)
- John A Calarco
National Institutes of Health (NIH award to Aravinthan Samuel)
- Aravinthan DT Samuel
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Reviewing Editor
- Eve Marder, Brandeis University, United States
Version history
- Received: August 25, 2016
- Accepted: November 14, 2016
- Accepted Manuscript published: November 18, 2016 (version 1)
- Version of Record published: November 23, 2016 (version 2)
- Version of Record updated: January 19, 2017 (version 3)
- Version of Record updated: March 8, 2017 (version 4)
Copyright
© 2016, Lim et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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Further reading
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