ArticleeLife2018
Motoneuron Wnts regulate neuromuscular junction development.
Article in eLife, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 56 citations in OpenAlex.
- A skeletal muscle atlas shows neuromuscular junction adaptations to growth and atrophy.Developmental cell · 2026Article
- Regulation of motor neuron differentiation in thebioRxiv : the preprint server for biology · 2025Article
- Crosstalk among canonical Wnt and Hippo pathway members in skeletal muscle and at the neuromuscular junction.Neural regeneration research · 2025Article
- Disrupted Motor Neuron and Neuromuscular Junction Development in an Albino Mice Model of Infantile Nystagmus.Investigative ophthalmology & visual science · 2025Article
- MBNL deficiency in motor neurons disrupts neuromuscular junction maintenance and gait coordination.Brain : a journal of neurology · 2025Article
- Sirt6 Mono-ADP-Ribosylates YY1 to Promote Dystrophin Expression for Neuromuscular Transmission.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The MuSK agonist antibody protects the neuromuscular junction and extends the lifespan in C9orf72-ALS mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Article
- Disruption of Neuromuscular Junction Following Spinal Cord Injury and Motor Neuron Diseases.International journal of molecular sciences · 2024Review
- Calcitriol ameliorates motor deficits and prolongs survival of Chrne-deficient mouse, a model for congenital myasthenic syndrome, by inducing Rspo2.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Article
- The impact of canonical Wnt transcriptional repressors TLE3 and TLE4 on postsynaptic transcription at the neuromuscular junction.Frontiers in molecular neuroscience · 2024Article
- C9orf72 poly-GA proteins impair neuromuscular transmission.Zoological research · 2023Article
- The role of Evi/Wntless in exporting Wnt proteins.Development (Cambridge, England) · 2023Review
- Intrafusal-fiber LRP4 for muscle spindle formation and maintenance in adult and aged animals.Nature communications · 2023Article
- FUS-ALS hiPSC-derived astrocytes impair human motor units through both gain-of-toxicity and loss-of-support mechanisms.Molecular neurodegeneration · 2023Article
- NMJ-related diseases beyond the congenital myasthenic syndromes.Frontiers in cell and developmental biology · 2023Review
- A link between agrin signalling and CaScientific reports · 2022Article
- Motoneurons innervation determines the distinct gene expressions in multinucleated myofibers.Cell & bioscience · 2022Article
- Post-synaptic specialization of the neuromuscular junction: junctional folds formation, function, and disorders.Cell & bioscience · 2022Review
- Transport and Secretion of the Wnt3 Ligand by Motor Neuron-like Cells and Developing Motor Neurons.Biomolecules · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 7 institutions in 2 countries.
Funding
Abstract
The neuromuscular junction (NMJ) is a synapse between motoneurons and skeletal muscles to control motor behavior. Unlike extensively investigated postsynaptic differentiation, less is known about mechanisms of presynaptic assembly. Genetic evidence of Wnt in mammalian NMJ development was missing due to the existence of multiple Wnts and their receptors. We show when Wnt secretion is abolished from motoneurons by mutating the Wnt ligand secretion mediator (Wls) gene, mutant mice showed muscle weakness and neurotransmission impairment. NMJs were unstable with reduced synaptic junctional folds and fragmented AChR clusters. Nerve terminals were swollen; synaptic vesicles were fewer and mislocated. The presynaptic deficits occurred earlier than postsynaptic deficits. Intriguingly, these phenotypes were not observed when deleting Wls in muscles or Schwann cells. We identified Wnt7A and Wnt7B as major Wnts for nerve terminal development in rescue experiments. These observations demonstrate a necessary role of motoneuron Wnts in NMJ development, in particular presynaptic differentiation.
Indexed as
Identifiers
What 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.