ArticleGenetics2006
Presynaptic UNC-31 (CAPS) is required to activate the G alpha(s) pathway of the Caenorhabditis elegans synaptic signaling network.
Article in Genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 102 citations in OpenAlex.
- Partitioning of the truncated insulin receptor DAF-2B between homodimers and heterodimers influences insulin signaling in C. elegans.PLoS genetics · 2026Article
- Auxin-inducible degradation of UNC-116 in C. elegans inhibits bidirectional dense core vesicle transport and worm locomotion on different timescales.Journal of cell science · 2026Article
- IGF-like growth factors that couple food sensing to developmental decisions employ different release mechanisms in a single pair ofbioRxiv : the preprint server for biology · 2026Article
- The insulin-like peptide INS-27 mediates a muscle-to-neuron feedback signal coupling muscle activity with AMPA receptor trafficking.PLoS genetics · 2025Article
- Loss of neuropeptidergic regulation of cholinergic transmission induces homeostatic compensation in muscle cells to preserve synaptic strength.PLoS biology · 2025Article
- TheThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- The exocytosis regulator complexin controls spontaneous synaptic vesicle release in a CAPS-dependent manner at C. elegans excitatory synapses.PLoS biology · 2025Article
- Article
- Cell non-autonomous signaling through the conserved C. elegans glycoprotein hormone receptor FSHR-1 regulates cholinergic neurotransmission.PLoS genetics · 2024Article
- Double mutation of open syntaxin and UNC-18 P334A leads to excitatory-inhibitory imbalance and impairs multiple aspects ofbioRxiv : the preprint server for biology · 2023Article
- Glial-derived mitochondrial signals affect neuronal proteostasis and aging.Science advances · 2023Article
- Inhibition of ribosome biogenesis in the epidermis is sufficient to trigger organism-wide growth quiescence independently of nutritional status in C. elegans.PLoS biology · 2023Article
- Conditional Degradation of UNC-31/CAPS Enables Spatiotemporal Analysis of Neuropeptide Function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Caenorhabditis elegans provides an efficient drug screening platform for GNAO1-related disorders and highlights the potential role of caffeine in controlling dyskinesia.Human molecular genetics · 2022Article
- Auxin-Inducible Degron System Reveals Temporal-Spatial Roles of HSF-1 and Its Transcriptional Program in Lifespan Assurance.Frontiers in aging · 2022Article
- Insulin/IGF-1 signaling and heat stress differentially regulate HSF1 activities in germline development.Cell reports · 2021Article
- Article
- Synapsin Is Required for Dense Core Vesicle Capture and cAMP-Dependent Neuropeptide Release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Open syntaxin overcomes exocytosis defects of diverse mutants in C. elegans.Nature communications · 2020Article
- Isolation and characterization of a novel member of the ACC ligand-gated chloride channel family, Hco-LCG-46, from the parasitic nematode Haemonchus contortus.Molecular and biochemical parasitology · 2020Article
4 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
C. elegans mutants lacking the dense-core vesicle priming protein UNC-31 (CAPS) share highly similar phenotypes with mutants lacking a neuronal G alpha(s) pathway, including strong paralysis despite exhibiting near normal levels of steady-state acetylcholine release as indicated by drug sensitivity assays. Our genetic analysis shows that UNC-31 and neuronal G alpha(s) are different parts of the same pathway and that the UNC-31/G alpha(s) pathway is functionally distinct from the presynaptic G alpha(q) pathway with which it interacts. UNC-31 acts upstream of G alpha(s) because mutations that activate the G alpha(s) pathway confer similar levels of strongly hyperactive, coordinated locomotion in both unc-31 null and (+) backgrounds. Using cell-specific promoters, we show that both UNC-31 and the G alpha(s) pathway function in cholinergic motor neurons to regulate locomotion rate. Using immunostaining we show that UNC-31 is often concentrated at or near active zones of cholinergic motor neuron synapses. Our data suggest that presynaptic UNC-31 activity, likely acting via dense-core vesicle exocytosis, is required to locally activate the neuronal G alpha(s) pathway near synaptic active zones.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.