ArticleDevelopmental cell2015
The E3 Ubiquitin Ligase TRIM9 Is a Filopodia Off Switch Required for Netrin-Dependent Axon Guidance.
Article in Developmental cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 103 citations in OpenAlex.
- Epigenome-wide Analysis Identifies Genes and Pathways Linked to Neurobehavioral Variation in Preterm Infants.Scientific reports · 2019Trial
- Review
- Coro1A and TRIM67 collaborate in netrin-dependent neuronal morphogenesis.The Journal of cell biology · 2025Article
- Structural analysis of TRIM family PRYSPRY domains and its implications for E3-ligand design.Journal of structural biology: X · 2025Article
- Article
- Emerging roles for E3 ubiquitin ligases in neural development and disease.Frontiers in cell and developmental biology · 2025Review
- TRIM9 Controls Growth Cone Responses to Netrin Through DCC and UNC5C.Journal of neurochemistry · 2025Article
- A human DCC variant causing mirror movement disorder reveals that the WAVE regulatory complex mediates axon guidance by netrin-1-DCC.Science signaling · 2024Article
- TRIM Proteins and Antiviral Microtubule Reorganization: A Novel Component in Innate Immune Responses?Viruses · 2024Review
- The E3 ubiquitin ligase TRIM9 regulates synaptic function and actin dynamics in response to netrin-1.Molecular biology of the cell · 2024Article
- Overview of epigenetic degraders based on PROTAC, molecular glue, and hydrophobic tagging technologies.Acta pharmaceutica Sinica. B · 2024Review
- Multi-monoubiquitylation controls VASP-mediated actin dynamics.Journal of cell science · 2024Article
- The E3 ubiquitin ligase TRIM9 regulates synaptic function and actin dynamics.bioRxiv : the preprint server for biology · 2024Article
- Netrin-1 stimulated axon growth requires the polyglutamylase TTLL1.Frontiers in neuroscience · 2024Article
- Targeted protein degradation in CNS disorders: a promising route to novel therapeutics?Frontiers in molecular neuroscience · 2024Review
- Loss of the E3 ubiquitin ligase TRIM67 alters the post-synaptic density proteome.microPublication biology · 2024Article
- Cardiomyocyte external mechanical unloading activates modifications of α-actinin differently from sarcomere-originated unloading.The FEBS journal · 2023Article
- Trim9 regulates the directional differentiation of retinal Müller cells to retinal ganglion cells.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023Article
- A twin UGUA motif directs the balance between gene isoforms through CFIm and the mTORC1 signaling pathway.eLife · 2023Article
- TRIM9 promotes Müller cell-derived retinal stem cells to differentiate into retinal ganglion cells by regulating Atoh7.In vitro cellular & developmental biology. Animal · 2023Article
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9 authors at 2 institutions in 2 countries.
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Abstract
Neuronal growth cone filopodia contain guidance receptors and contribute to axon guidance; however, the mechanism by which the guidance cue netrin increases filopodia density is unknown. Here, we demonstrate that TRIM9, an E3 ubiquitin ligase that localizes to filopodia tips and binds the netrin receptor DCC, interacts with and ubiquitinates the barbed-end polymerase VASP to modulate filopodial stability during netrin-dependent axon guidance. Studies with murine Trim9(+/+) and Trim9(-/-) cortical neurons, along with a non-ubiquitinatable VASP mutant, demonstrate that TRIM9-mediated ubiquitination of VASP reduces VASP filopodial tip localization, VASP dynamics at tips, and filopodial stability. Upon netrin treatment, VASP is deubiquitinated, which promotes VASP tip localization and filopodial stability. Trim9 deletion induces axon guidance defects in vitro and in vivo, whereas a gradient of deubiquitinase inhibition promotes axon turning in vitro. We conclude that a gradient of TRIM9-mediated ubiquitination of VASP creates a filopodial stability gradient during axon turning.
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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.