ArticleNature communications2014
VAV-1 acts in a single interneuron to inhibit motor circuit activity in Caenorhabditis elegans.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
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- Axon-Dependent Patterning and Maintenance of Somatosensory Dendritic Arbors.Developmental cell · 2019Article
- Blue-Light Receptors for Optogenetics.Chemical reviews · 2018Review
- Regulation of Glutamate Signaling in the Sensorimotor Circuit by CASY-1A/Calsyntenin inGenetics · 2018Article
- Glia Modulate a Neuronal Circuit for Locomotion Suppression during Sleep in C. elegans.Cell reports · 2018Article
- The C-terminal of CASY-1/Calsyntenin regulates GABAergic synaptic transmission at the Caenorhabditis elegans neuromuscular junction.PLoS genetics · 2018Article
- The Sleep in Caenorhabditis elegans: What We Know Until Now.Molecular neurobiology · 2018Review
- Neuroendocrine modulation sustains theeLife · 2016Article
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- A Conserved GEF for Rho-Family GTPases Acts in an EGF Signaling Pathway to Promote Sleep-like Quiescence in Caenorhabditis elegans.Genetics · 2016Article
- Highly efficient optogenetic cell ablation in C. elegans using membrane-targeted miniSOG.Scientific reports · 2016Article
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
The complex molecular and cellular mechanisms underlying neuronal control of animal movement are not well understood. Locomotion of Caenorhabditis elegans is mediated by a neuronal circuit that produces coordinated sinusoidal movement. Here we utilize this simple, yet elegant, behaviour to show that VAV-1, a conserved guanine nucleotide exchange factor for Rho-family GTPases, negatively regulates motor circuit activity and the rate of locomotion. While vav-1 is expressed in a small subset of neurons, we find that VAV-1 function is required in a single interneuron, ALA, to regulate motor neuron circuit activity. Furthermore, we show by genetic and optogenetic manipulation of ALA that VAV-1 is required for the excitation and activation of this neuron. We find that ALA signalling inhibits command interneuron activity by abrogating excitatory signalling in the command interneurons, which is responsible for promoting motor neuron circuit activity. Together, our data describe a novel neuromodulatory role for VAV-1-dependent signalling in the regulation of motor circuit activity and locomotion.
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