ArticleHuman molecular genetics2015
Glial TDP-43 regulates axon wrapping, GluRIIA clustering and fly motility by autonomous and non-autonomous mechanisms.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- Loss of TDP-43 Drives Innate Immune Activation Through Relish inInternational journal of molecular sciences · 2026Article
- TDP-43 Regulates Rab4 Levels to Support Synaptic Vesicle Recycling and Neuromuscular Connectivity inInternational journal of molecular sciences · 2025Article
- Su(var)3-9 mediates age-dependent increase in H3K9 methylation on TDP-43 promoter triggering neurodegeneration.Cell death discovery · 2023Article
- Review
- Fly for ALS: Drosophila modeling on the route to amyotrophic lateral sclerosis modifiers.Cellular and molecular life sciences : CMLS · 2021Review
- Immuno-electrophysiology on Neuromuscular Junctions of Drosophila Third Instar Larva.Bio-protocol · 2021Article
- Amyotrophic Lateral Sclerosis Genes inInternational journal of molecular sciences · 2021Review
- Review
- TDP-43 prevents retrotransposon activation in the Drosophila motor system through regulation of Dicer-2 activity.BMC biology · 2020Article
- TDP-43 promotes the formation of neuromuscular synapses through the regulation of Disc-large expression in Drosophila skeletal muscles.BMC biology · 2020Article
- Glial Cells-The Strategic Targets in Amyotrophic Lateral Sclerosis Treatment.Journal of clinical medicine · 2020Review
- SQuIRE reveals locus-specific regulation of interspersed repeat expression.Nucleic acids research · 2019Article
- Downregulation of glutamic acid decarboxylase in Drosophila TDP-43-null brains provokes paralysis by affecting the organization of the neuromuscular synapses.Scientific reports · 2018Article
- Overexpression ofAmerican journal of neurodegenerative disease · 2018Article
- TDP-43 Depletion in Microglia Promotes Amyloid Clearance but Also Induces Synapse Loss.Neuron · 2017Article
- Retrotransposon activation contributes to neurodegeneration in a Drosophila TDP-43 model of ALS.PLoS genetics · 2017Article
- Failure to Deliver and Translate-New Insights into RNA Dysregulation in ALS.Frontiers in cellular neuroscience · 2017Review
- Role and Therapeutic Potential of Astrocytes in Amyotrophic Lateral Sclerosis.Current pharmaceutical design · 2017Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alterations in the glial function of TDP-43 are becoming increasingly associated with the neurological symptoms observed in Amyotrophic Lateral Sclerosis (ALS), however, the physiological role of this protein in the glia or the mechanisms that may lead to neurodegeneration are unknown. To address these issues, we modulated the expression levels of TDP-43 in the Drosophila glia and found that the protein was required to regulate the subcellular wrapping of motoneuron axons, promote synaptic growth and the formation of glutamate receptor clusters at the neuromuscular junctions. Interestingly, we determined that the glutamate transporter EAAT1 mediated the regulatory functions of TDP-43 in the glia and demonstrated that genetic or pharmacological compensations of EAAT1 activity were sufficient to modulate glutamate receptor clustering and locomotive behaviors in flies. The data uncovers autonomous and non-autonomous functions of TDP-43 in the glia and suggests new experimentally based therapeutic strategies in ALS.
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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.