ArticleThe Journal of cell biology2020
α-Tubulin detyrosination impairs mitotic error correction by suppressing MCAK centromeric activity.
Article in The Journal of cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 52 citations in OpenAlex.
- Post-Translational Modifications of Tubulin in Oocyte Maturation and Female Infertility.Cytoskeleton (Hoboken, N.J.) · 2026Review
- Condensation of MATCAP promotes CENP-E-dependent chromosome congression in mitosis.Nature communications · 2026Article
- Prognostic, diagnostic and therapeutic value of the cancer tubulin code.Cancer metastasis reviews · 2026Review
- MATCAP1 preferentially binds an expanded tubulin conformation to generate detyrosinated and ΔC2 α-tubulin.The EMBO journal · 2026Article
- Emerging Roles of Tubulin Isoforms and Their Post-Translational Modifications in Microtubule-Based Transport and Cellular Functions.Biomolecules · 2026Review
- How does the tubulin code facilitate directed cell migration?Biochemical Society transactions · 2025Review
- α-tubulin detyrosination fine-tunes kinetochore-microtubule attachments.Nature communications · 2024Article
- BUB1B monoallelic germline variants contribute to prostate cancer predisposition by triggering chromosomal instability.Journal of biomedical science · 2024Article
- Δ3-tubulin impairs mitotic spindle morphology and increases nuclear size in pancreatic cancer cells.Medical molecular morphology · 2024Article
- Microtubule detyrosination drives symmetry breaking to polarize cells for directed cell migration.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Initial spindle positioning at the oocyte center protects against incorrect kinetochore-microtubule attachment and aneuploidy in mice.Science advances · 2023Article
- Mechanistic Analysis of CCP1 in Generating ΔC2 α-Tubulin in Mammalian Cells and Photoreceptor Neurons.Biomolecules · 2023Article
- α-Tubulin detyrosination links the suppression of MCAK activity with taxol cytotoxicity.The Journal of cell biology · 2023Article
- Chromosome segregation fidelity requires microtubule polyglutamylation by the cancer downregulated enzyme TTLL11.Nature communications · 2022Article
- Tension of plus-end tracking protein Clip170 confers directionality and aggressiveness during breast cancer migration.Cell death & disease · 2022Article
- Augmin-dependent microtubule self-organization drives kinetochore fiber maturation in mammals.Cell reports · 2022Article
- Article
- TH588 and Low-Dose Nocodazole Impair Chromosome Congression by Suppressing Microtubule Turnover within the Mitotic Spindle.Cancers · 2021Article
- Article
- Chromosome oscillation promotes Aurora A-dependent Hec1 phosphorylation and mitotic fidelity.The Journal of cell biology · 2021Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Incorrect kinetochore-microtubule attachments during mitosis can lead to chromosomal instability, a hallmark of human cancers. Mitotic error correction relies on the kinesin-13 MCAK, a microtubule depolymerase whose activity in vitro is suppressed by α-tubulin detyrosination-a posttranslational modification enriched on long-lived microtubules. However, whether and how MCAK activity required for mitotic error correction is regulated by α-tubulin detyrosination remains unknown. Here we found that detyrosinated α-tubulin accumulates on correct, more stable, kinetochore-microtubule attachments. Experimental manipulation of tubulin tyrosine ligase (TTL) or carboxypeptidase (Vasohibins-SVBP) activities to constitutively increase α-tubulin detyrosination near kinetochores compromised efficient error correction, without affecting overall kinetochore microtubule stability. Rescue experiments indicate that MCAK centromeric activity was required and sufficient to correct the mitotic errors caused by excessive α-tubulin detyrosination independently of its global impact on microtubule dynamics. Thus, microtubules are not just passive elements during mitotic error correction, and the extent of α-tubulin detyrosination allows centromeric MCAK to discriminate correct vs. incorrect kinetochore-microtubule attachments, thereby promoting mitotic fidelity.
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