ArticleeLife2016
Acetylated tubulin is essential for touch sensation in mice.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 103 citations in OpenAlex.
- Microtubule Cytoskeleton Dysfunction in Chronic Pain: Mechanisms of Transport Failure and Emerging Therapeutic Targets.International journal of molecular sciences · 2026Review
- Mutating different α-tubulin acetylation sites has distinct effects on axon terminal morphogenesis inMolecular biology of the cell · 2026Article
- Prognostic, diagnostic and therapeutic value of the cancer tubulin code.Cancer metastasis reviews · 2026Review
- OptoTAT reveals microtubule acetylation as a rapid trigger for GEF-H1-mediated cell migration.The Journal of cell biology · 2026Article
- Time-Restricted Feeding Alters Behavior in a Sex-Specific Manner in Mice With Neuropathic Pain.Molecular nutrition & food research · 2026Article
- Spinal cord Tau pathology induces tactile deficits and cognitive impairment in Alzheimer's disease via dysregulation of CCK neurons.Nature neuroscience · 2026Article
- Mutating different α-tubulin acetylation sites has distinct effects on axon terminal morphogenesis inbioRxiv : the preprint server for biology · 2025Article
- Obstacles Regulate Membrane Tension Propagation to Enable Localized Mechanotransduction.bioRxiv : the preprint server for biology · 2025Article
- Recombinant Monoclonal Antibodies for Detecting the Tubulin Post-Translational Modifications Glutamylation and Lysine-40 Acetylation.Cytoskeleton (Hoboken, N.J.) · 2025Article
- How does the tubulin code facilitate directed cell migration?Biochemical Society transactions · 2025Review
- Tubulin acetyltransferases access and modify the microtubule luminal K40 residue through anchors in taxane-binding pockets.Nature structural & molecular biology · 2025Article
- Emerging roles for tubulin PTMs in neuronal function and neurodegenerative disease.Current opinion in neurobiology · 2025Review
- Tubulin Acetylation and the Cellular Mechanosensing and Stress Response.Results and problems in cell differentiation · 2025Review
- Optogenetically Induced Microtubule Acetylation Unveils the Molecular Dynamics of Actin-Microtubule Crosstalk in Directed Cell Migration.bioRxiv : the preprint server for biology · 2024Article
- Extracellular signals induce dynamic ER remodeling through αTAT1-dependent microtubule acetylation.Neoplasia (New York, N.Y.) · 2024Article
- MFN2 coordinates mitochondria motility with α-tubulin acetylation and this regulation is disrupted in CMT2A.iScience · 2024Article
- The local mechanosensitive response of primary cardiac fibroblasts is influenced by the microenvironment mechanics.Scientific reports · 2024Article
- A missense mutation in human INSC causes peripheral neuropathy.EMBO molecular medicine · 2024Article
- The α-tubulin acetyltransferase ATAT1: structure, cellular functions, and its emerging role in human diseases.Cellular and molecular life sciences : CMLS · 2024Review
- VAP spatially stabilizes dendritic mitochondria to locally support synaptic plasticity.Nature communications · 2024Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
25 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
At its most fundamental level, touch sensation requires the translation of mechanical energy into mechanosensitive ion channel opening, thereby generating electro-chemical signals. Our understanding of this process, especially how the cytoskeleton influences it, remains unknown. Here we demonstrate that mice lacking the α-tubulin acetyltransferase Atat1 in sensory neurons display profound deficits in their ability to detect mechanical stimuli. We show that all cutaneous afferent subtypes, including nociceptors have strongly reduced mechanosensitivity upon Atat1 deletion, and that consequently, mice are largely insensitive to mechanical touch and pain. We establish that this broad loss of mechanosensitivity is dependent upon the acetyltransferase activity of Atat1, which when absent leads to a decrease in cellular elasticity. By mimicking α-tubulin acetylation genetically, we show both cellular rigidity and mechanosensitivity can be restored in Atat1 deficient sensory neurons. Hence, our results indicate that by influencing cellular stiffness, α-tubulin acetylation sets the force required for touch.
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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.