ArticleDisease models & mechanisms2016
Tau excess impairs mitosis and kinesin-5 function, leading to aneuploidy and cell death.
Article in Disease models & mechanisms, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 46 citations in OpenAlex.
- Microtubule stiffening by the doublecortin-domain protein ZYG-8 contributes to mitotic spindle orientation during zygote division in Caenorhabditis elegans.PLoS genetics · 2026Article
- Drosophila wing is a high-throughput and versatile screening tool for Tau-mediated disease mechanisms and drug discovery.Disease models & mechanisms · 2026Article
- Tau condensation on DNA mediates microtubule attachment suggesting a mitotic role for centromere-localized tau.Nature communications · 2026Article
- Article
- High Tau expression correlates with reduced invasion and prolonged survival in Ewing sarcoma.Cell death discovery · 2025Article
- Eg5 and Diseases: From the Well-Known Role in Cancer to the Less-Known Activity in Noncancerous Pathological Conditions.Biochemistry research international · 2024Review
- Mitotic phosphorylation of Tau/MAPT modulates cell cycle progression in prostate cancer cells.Journal of cancer research and clinical oncology · 2023Article
- Kinesin-5 Eg5 is essential for spindle assembly, chromosome stability and organogenesis in development.Cell death discovery · 2022Article
- IncreasediScience · 2022Article
- Review
- Article
- Tau oligomers accumulation sensitizes prostate cancer cells to docetaxel treatment.Journal of cancer research and clinical oncology · 2021Article
- Novel function ofProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Emerging Evidences for an Implication of the Neurodegeneration-Associated Protein TAU in Cancer.Brain sciences · 2020Review
- Phase Separation in Cell Division.Molecular cell · 2020Review
- Tau and Alpha Synuclein Synergistic Effect in Neurodegenerative Diseases: When the Periphery Is the Core.International journal of molecular sciences · 2020Review
- Cell Cycle Deficits in Neurodegenerative Disorders: Uncovering Molecular Mechanisms to Drive Innovative Therapeutic Development.Aging and disease · 2020Review
- Developmental Pathogenicity of 4-Repeat Human Tau Is Lost with the P301L Mutation in Genetically Matched Tau-Transgenic Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Plasma Neurofilament Light Chain May Be a Biomarker for the Inverse Association Between Cancers and Neurodegenerative Diseases.Frontiers in aging neuroscience · 2020Article
- ADAMTS Sol narae cleaves extracellular Wingless to generate a novel active form that regulates cell proliferation in Drosophila.Cell death & disease · 2019Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In neurodegenerative diseases such as Alzheimer's disease (AD), cell cycle defects and associated aneuploidy have been described. However, the importance of these defects in the physiopathology of AD and the underlying mechanistic processes are largely unknown, in particular with respect to the microtubule (MT)-binding protein Tau, which is found in excess in the brain and cerebrospinal fluid of affected individuals. Although it has long been known that Tau is phosphorylated during mitosis to generate a lower affinity for MTs, there is, to our knowledge, no indication that an excess of this protein could affect mitosis. Here, we studied the effect of an excess of human Tau (hTau) protein on cell mitosis in vivo. Using the Drosophila developing wing disc epithelium as a model, we show that an excess of hTau induces a mitotic arrest, with the presence of monopolar spindles. This mitotic defect leads to aneuploidy and apoptotic cell death. We studied the mechanism of action of hTau and found that the MT-binding domain of hTau is responsible for these defects. We also demonstrate that the effects of hTau occur via the inhibition of the function of the kinesin Klp61F, the Drosophila homologue of kinesin-5 (also called Eg5 or KIF11). We finally show that this deleterious effect of hTau is also found in other Drosophila cell types (neuroblasts) and tissues (the developing eye disc), as well as in human HeLa cells. By demonstrating that MT-bound Tau inhibits the Eg5 kinesin and cell mitosis, our work provides a new framework to consider the role of Tau in neurodegenerative diseases.
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