ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Regulation of neurotransmitter vesicles by the homeodomain protein UNC-4 and its transcriptional corepressor UNC-37/groucho in Caenorhabditis elegans cholinergic motor neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 73 citations in OpenAlex.
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- Preconditioning of Caenorhabditis elegans to anoxic insult by inactivation of cholinergic, GABAergic and muscle activity.Genes, brain, and behavior · 2021Article
- The Conserved ASCL1/MASH-1 Ortholog HLH-3 Specifies Sex-Specific Ventral Cord Motor Neuron Fate inG3 (Bethesda, Md.) · 2020Article
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- High-Content Microfluidic Screening Platform Used To Identify σ2R/Tmem97 Binding Ligands that Reduce Age-Dependent Neurodegeneration in C. elegans SC_APP Model.ACS chemical neuroscience · 2018Article
- FLP-18 Functions through the G-Protein-Coupled Receptors NPR-1 and NPR-4 to Modulate Reversal Length inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Research and progress on ClC‑2 (Review).Molecular medicine reports · 2017Review
- The secreted MSP domain ofDevelopment (Cambridge, England) · 2017Article
- TheDevelopment (Cambridge, England) · 2017Article
- A map of terminal regulators of neuronal identity in Caenorhabditis elegans.Wiley interdisciplinary reviews. Developmental biology · 2016Review
- Transcriptional coordination of synaptogenesis and neurotransmitter signaling.Current biology : CB · 2015Article
- A novel nondevelopmental role of the sax-7/L1CAM cell adhesion molecule in synaptic regulation in Caenorhabditis elegans.Genetics · 2015Article
- The voltage-gated anion channels encoded by clh-3 regulate egg laying in C. elegans by modulating motor neuron excitability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Large-scale gene knockdown in C. elegans using dsRNA feeding libraries to generate robust loss-of-function phenotypes.Journal of visualized experiments : JoVE · 2013Article
- A method for culturing embryonic C. elegans cells.Journal of visualized experiments : JoVE · 2013Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Motor neuron function depends on neurotransmitter release from synaptic vesicles (SVs). Here we show that the UNC-4 homeoprotein and its transcriptional corepressor protein UNC-37 regulate SV protein levels in specific Caenorhabditis elegans motor neurons. UNC-4 is expressed in four classes (DA, VA, VC, and SAB) of cholinergic motor neurons. Antibody staining reveals that five different vesicular proteins (UNC-17, choline acetyltransferase, Synaptotagmin, Synaptobrevin, and RAB-3) are substantially reduced in unc-4 and unc-37 mutants in these cells; nonvesicular neuronal proteins (Syntaxin, UNC-18, and UNC-11) are not affected, however. Ultrastructural analysis of VA motor neurons in the mutant unc-4(e120) confirms that SV number in the presynaptic zone is reduced ( approximately 40%) whereas axonal diameter and synaptic morphology are not visibly altered. Because the UNC-4-UNC-37 complex has been shown to mediate transcriptional repression, we propose that these effects are performed via an intermediate gene. Our results are consistent with a model in which this unc-4 target gene ("gene-x") functions at a post-transcriptional level as a negative regulator of SV biogenesis or stability. Experiments with a temperature-sensitive unc-4 mutant show that the adult level of SV proteins strictly depends on unc-4 function during a critical period of motor neuron differentiation. unc-4 activity during this sensitive larval stage is also required for the creation of proper synaptic inputs to VA motor neurons. The temporal correlation of these events may mean that a common unc-4-dependent mechanism controls both the specificity of synaptic inputs as well as the strength of synaptic outputs for these motor neurons.
Indexed as
Identifiers
11245684PMC6762608W1612484725What OpenQuestion holds
Registered trials
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.