ArticleProceedings of the National Academy of Sciences of the United States of America2011
Interaction of survival of motor neuron (SMN) and HuD proteins with mRNA cpg15 rescues motor neuron axonal deficits.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.
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Who cites it
137 citing papers in PubMed, 196 citations in OpenAlex.
- A Comparative Study of SMN Protein and mRNA in Blood and Fibroblasts in Patients with Spinal Muscular Atrophy and Healthy Controls.PloS one · 2016Trial
- ELAVL Proteins, miRNA Fate, and Extracellular RNA Communication in Brain Aging and Neurodegeneration.Cells · 2026Review
- Full thickness three-dimensional mapping of neuronal populations within the avian enteric nervous system.Poultry science · 2026Article
- Circular RNAs in Neurons: From Transport to Function.Non-coding RNA · 2026Review
- 3'UTR regulation of axon translation and optic nerve regeneration.Molecular neurodegeneration · 2026Article
- Multiple mTOR RNA localization signals regulate subcellular protein synthesis and axonal growth.bioRxiv : the preprint server for biology · 2026Article
- Immaturity of the neuromuscular junction in spinal muscular atrophy mouse models.Frontiers in cellular neuroscience · 2026Review
- KHSRP-mediated decay of axonally localized prenyl-Cdc42 mRNA slows nerve regeneration.PLoS genetics · 2025Article
- Sm-site containing mRNAs can accept Sm-rings and are downregulated in Spinal Muscular Atrophy.Nucleic acids research · 2025Article
- The Antidepressant Effect of Resveratrol Is Related to Neuroplasticity Mediated by the ELAVL4-International journal of molecular sciences · 2025Article
- The SMN-ribosome interplay: a new opportunity for Spinal Muscular Atrophy therapies.Biochemical Society transactions · 2024Review
- Modeling Spinal Muscular Atrophy in Zebrafish: Current Advances and Future Perspectives.International journal of molecular sciences · 2024Review
- Mitigating aberrant Cdk5 activation alleviates mitochondrial defects and motor neuron disease symptoms in spinal muscular atrophy.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- PRMT inhibitor promotes SMN2 exon 7 inclusion and synergizes with nusinersen to rescue SMA mice.EMBO molecular medicine · 2023Article
- RNA trafficking and subcellular localization-a review of mechanisms, experimental and predictive methodologies.Briefings in bioinformatics · 2023Review
- Innovating spinal muscular atrophy models in the therapeutic era.Disease models & mechanisms · 2023Article
- SMN promotes mitochondrial metabolic maturation during myogenesis by regulating the MYOD-miRNA axis.Life science alliance · 2023Article
- The SMN Complex at the Crossroad between RNA Metabolism and Neurodegeneration.International journal of molecular sciences · 2023Review
- SMN post-translational modifications in spinal muscular atrophy.Frontiers in cellular neuroscience · 2023Review
- Emerging Roles for the RNA-Binding Protein HuD (ELAVL4) in Nervous System Diseases.International journal of molecular sciences · 2022Review
77 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Spinal muscular atrophy (SMA), caused by the deletion of the SMN1 gene, is the leading genetic cause of infant mortality. SMN protein is present at high levels in both axons and growth cones, and loss of its function disrupts axonal extension and pathfinding. SMN is known to associate with the RNA-binding protein hnRNP-R, and together they are responsible for the transport and/or local translation of β-actin mRNA in the growth cones of motor neurons. However, the full complement of SMN-interacting proteins in neurons remains unknown. Here we used mass spectrometry to identify HuD as a novel neuronal SMN-interacting partner. HuD is a neuron-specific RNA-binding protein that interacts with mRNAs, including candidate plasticity-related gene 15 (cpg15). We show that SMN and HuD form a complex in spinal motor axons, and that both interact with cpg15 mRNA in neurons. CPG15 is highly expressed in the developing ventral spinal cord and can promote motor axon branching and neuromuscular synapse formation, suggesting a crucial role in the development of motor axons and neuromuscular junctions. Cpg15 mRNA previously has been shown to localize into axonal processes. Here we show that SMN deficiency reduces cpg15 mRNA levels in neurons, and, more importantly, cpg15 overexpression partially rescues the SMN-deficiency phenotype in zebrafish. Our results provide insight into the function of SMN protein in axons and also identify potential targets for the study of mechanisms that lead to the SMA pathology and related neuromuscular diseases.
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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.