ArticleMolecular neurodegeneration2010
High-efficiency transfection of cultured primary motor neurons to study protein localization, trafficking, and function.
Article in Molecular neurodegeneration, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 74 citations in OpenAlex.
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- Therapeutic strategies for spinal muscular atrophy: the history and future perspective.Frontiers in human neuroscience · 2026Review
- Improved CaP Nanoparticles for Nucleic Acid and Protein Delivery to Neural Primary Cultures and Stem Cells.ACS nano · 2024Article
- SMN post-translational modifications in spinal muscular atrophy.Frontiers in cellular neuroscience · 2023Review
- SMN Is Physiologically Downregulated at Wild-Type Motor Nerve Terminals but Aggregates Together with Neurofilaments in SMA Mouse Models.Biomolecules · 2022Article
- ALS-associated KIF5A mutations abolish autoinhibition resulting in a toxic gain of function.Cell reports · 2022Article
- A primary rodent triculture model to investigate the role of glia-neuron crosstalk in regulation of neuronal activity.Frontiers in aging neuroscience · 2022Article
- Oligonucleotides Targeting DNA Repeats DownregulateNucleic acid therapeutics · 2021Article
- FUS-ALS mutants alter FMRP phase separation equilibrium and impair protein translation.Science advances · 2021Article
- Functional Abnormalities of Cerebellum and Motor Cortex in Spinal Muscular Atrophy Mice.Neuroscience · 2021Article
- Fluorescence Correlation Spectroscopy Reveals Survival Motor Neuron Oligomerization but No Active Transport in Motor Axons of a Zebrafish Model for Spinal Muscular Atrophy.Frontiers in cell and developmental biology · 2021Article
- Smcr8 deficiency disrupts axonal transport-dependent lysosomal function and promotes axonal swellings and gain of toxicity in C9ALS/FTD mouse models.Human molecular genetics · 2019Article
- Distal denervation in the SOD1 knockout mouse correlates with loss of mitochondria at the motor nerve terminal.Experimental neurology · 2019Article
- Estimating transfection efficiency in differentiated and undifferentiated neural cells.BMC research notes · 2019Article
- The Alteration of Intrinsic Excitability and Synaptic Transmission in Lumbar Spinal Motor Neurons and Interneurons of Severe Spinal Muscular Atrophy Mice.Frontiers in cellular neuroscience · 2019Article
- mRNP assembly, axonal transport, and local translation in neurodegenerative diseases.Brain research · 2018Review
- TDP-43 pathology disrupts nuclear pore complexes and nucleocytoplasmic transport in ALS/FTD.Nature neuroscience · 2018Article
- Post-transcriptional Inhibition of Hsc70-4/HSPA8 Expression Leads to Synaptic Vesicle Cycling Defects in Multiple Models of ALS.Cell reports · 2017Article
- Therapeutic strategies for spinal muscular atrophy: SMN and beyond.Disease models & mechanisms · 2017Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCultured spinal motor neurons are a valuable tool to study basic mechanisms of development, axon growth and pathfinding, and, importantly, to analyze the pathomechanisms underlying motor neuron diseases. However, the application of this cell culture model is limited by the lack of efficient gene transfer techniques which are available for other neurons. To address this problem, we have established magnetofection as a novel method for the simple and efficient transfection of mouse embryonic motor neurons. This technique allows for the study of the effects of gene expression and silencing on the development and survival of motor neurons.
resultsWe found that magnetofection, a novel transfection technology based on the delivery of DNA-coated magnetic nanobeads, can be used to transfect primary motor neurons. Therefore, in order to use this method as a new tool for studying the localization and transport of axonal proteins, we optimized conditions and determined parameters for efficient transfection rates of >45% while minimizing toxic effects on survival and morphology. To demonstrate the potential of this method, we have used transfection with plasmids encoding fluorescent fusion-proteins to show for the first time that the spinal muscular atrophy-disease protein Smn is actively transported along axons of live primary motor neurons, supporting an axon-specific role for Smn that is different from its canonical function in mRNA splicing. We were also able to show the suitability of magnetofection for gene knockdown with shRNA-based constructs by significantly reducing Smn levels in both cell bodies and axons, opening new opportunities for the study of the function of axonal proteins in motor neurons.
conclusionsIn this study we have established an optimized magnetofection protocol as a novel transfection method for primary motor neurons that is simple, efficient and non-toxic. We anticipate that this novel approach will have a broad applicability in the study of motor neuron development, axonal trafficking, and molecular mechanisms of motor neuron 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.