ArticleThe EMBO journal2021
Distinct roles of α- and β-tubulin polyglutamylation in controlling axonal transport and in neurodegeneration.
Article in The EMBO journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 36 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
36 citing papers in PubMed, 53 citations in OpenAlex.
- Microtubule posttranslational modifications provide unique recognition patterns for associated proteins.The EMBO journal · 2026Article
- Towards a systems-level view of the microtubule cytoskeleton and its functions in physiology and disease.Nature reviews. Molecular cell biology · 2026Review
- Post-Translational Modifications of Tubulin in Oocyte Maturation and Female Infertility.Cytoskeleton (Hoboken, N.J.) · 2026Review
- Structural Basis of Human Kinetochore-Microtubule Coupling by the Ndc80 and Ska Complexes.bioRxiv : the preprint server for biology · 2026Article
- Prognostic, diagnostic and therapeutic value of the cancer tubulin code.Cancer metastasis reviews · 2026Review
- Identification of a component of the tubulin poly-glutamylase complex required for phosphoinositide homeostasis and cilium assembly and maintenance.Nature communications · 2026Article
- TPGS1 regulates central spindle microtubule glutamylation and remodeling during telophase and abscission.EMBO reports · 2026Article
- Computational perspectives on tubulin E-hook structure and mechanisms.Biophysical reports · 2026Review
- Emerging Roles of Tubulin Isoforms and Their Post-Translational Modifications in Microtubule-Based Transport and Cellular Functions.Biomolecules · 2026Review
- Article
- Recombinant Monoclonal Antibodies for Detecting the Tubulin Post-Translational Modifications Glutamylation and Lysine-40 Acetylation.Cytoskeleton (Hoboken, N.J.) · 2025Article
- Genomics reveals eleven obesity endotypes with distinct biological and phenotypic signatures.medRxiv : the preprint server for health sciences · 2025Article
- Polyglutamylation of microtubules drives neuronal remodeling.Nature communications · 2025Article
- Doublecortin restricts neuronal branching by regulating tubulin polyglutamylation.Nature communications · 2025Article
- Emerging roles for tubulin PTMs in neuronal function and neurodegenerative disease.Current opinion in neurobiology · 2025Review
- Glutamylation imbalance impairs the molecular architecture of the photoreceptor cilium.The EMBO journal · 2024Article
- Article
- Netrin-1 stimulated axon growth requires the polyglutamylase TTLL1.Frontiers in neuroscience · 2024Article
- Zn2+ decoration of microtubules arrests axonal transport and displaces tau, doublecortin, and MAP2C.The Journal of cell biology · 2023Article
- The distinct initiation sites and processing activities of TTLL4 and TTLL7 in glutamylation of brain tubulin.The Journal of biological chemistry · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tubulin polyglutamylation is a post-translational modification of the microtubule cytoskeleton, which is generated by a variety of enzymes with different specificities. The "tubulin code" hypothesis predicts that modifications generated by specific enzymes selectively control microtubule functions. Our recent finding that excessive accumulation of polyglutamylation in neurons causes their degeneration and perturbs axonal transport provides an opportunity for testing this hypothesis. By developing novel mouse models and a new glutamylation-specific antibody, we demonstrate here that the glutamylases TTLL1 and TTLL7 generate unique and distinct glutamylation patterns on neuronal microtubules. We find that under physiological conditions, TTLL1 polyglutamylates α-tubulin, while TTLL7 modifies β-tubulin. TTLL1, but not TTLL7, catalyses the excessive hyperglutamylation found in mice lacking the deglutamylase CCP1. Consequently, deletion of TTLL1, but not of TTLL7, prevents degeneration of Purkinje cells and of myelinated axons in peripheral nerves in these mice. Moreover, loss of TTLL1 leads to increased mitochondria motility in neurons, while loss of TTLL7 has no such effect. By revealing how specific patterns of tubulin glutamylation, generated by distinct enzymes, translate into specific physiological and pathological readouts, we demonstrate the relevance of the tubulin code for homeostasis.
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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.