ArticleFrontiers in aging2023
Pathogenic tau decreases nuclear tension in cultured neurons.
Article in Frontiers in aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Elevation of the mechanically-sensitive e protein emerin links nuclear mechanotransduction to tau-induced cytoskeletal remodeling in neurons.Nucleus (Austin, Tex.) · 2026Article
- Nuclear membrane disruption in neurodegenerative diseases: Emerging perspectives.Neural regeneration research · 2026Article
- Nuclear dysfunction in aging and neurodegeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Tau oligomerization induces nuclear lamina invagination and chromatin remodeling in Alzheimer's disease.Acta neuropathologica · 2026Article
- Neuromechanobiology: Bridging Mechanobiology and Neuroscience Through Evidence and Open Questions.Cells · 2026Review
- Stress transmission towards the nucleus of the cell.Frontiers in cell and developmental biology · 2026Review
- Elevation of the mechanically-sensitive protein emerin links nuclear mechanotransduction to tau-induced cytoskeletal remodeling in neurons.bioRxiv : the preprint server for biology · 2025Article
- A phenotypic screen for novel small molecules that correct tau-mediated pathologies in human frontotemporal dementia neurons.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Cell redistribution of G quadruplex-structured DNA is associated with morphological changes of nuclei and nucleoli in neurons during tau pathology progression.Brain pathology (Zurich, Switzerland) · 2025Article
- Using ALS to understand profilin 1's diverse roles in cellular physiology.Cytoskeleton (Hoboken, N.J.) · 2025Review
- Spatial transcriptomics reveals an unexpected impact of tau and tau pathology on the expression of transthyretin.Frontiers in aging neuroscience · 2025Article
- Cellular and pathological functions of tau.Nature reviews. Molecular cell biology · 2024Review
- A novel role for CSA in the regulation of nuclear envelope integrity: uncovering a non-canonical function.Life science alliance · 2024Article
- Pathogenic tau induces an adaptive elevation in mRNA translation rate at early stages of disease.Aging cell · 2024Article
- Biomaterials Mimicking Mechanobiology: A Specific Design for a Specific Biological Application.International journal of molecular sciences · 2024Review
- Phosphorylation regulates tau's phase separation behavior and interactions with chromatin.Communications biology · 2024Article
- m6A-dependent circular RNA formation mediates tau-induced neurotoxicity.bioRxiv : the preprint server for biology · 2024Article
- Phosphorylation regulates tau's phase separation behavior and interactions with chromatin.bioRxiv : the preprint server for biology · 2023Article
- Reply: Soluble oligomers or insoluble fibrils?Acta neuropathologica · 2023Article
- Alzheimer's disease and related tauopathies: disorders of disrupted neuronal identity.Trends in neurosciences · 2023Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Neurodegenerative tauopathies, including Alzheimer's disease, are pathologically defined by the presence of aggregated forms of tau protein in brains of affected individuals. Previous studies report that the negative effects of pathogenic tau on the actin cytoskeleton and microtubules cause a toxic destabilization of the lamin nucleoskeleton and formation of nuclear invaginations and blebs. Based on the known function of the nucleus as a mechanosensor, as well as the high incidence of nuclear pleomorphism in human Alzheimer's disease and related tauopathies, we investigated the effects of pathogenic tau on nuclear tension. We first find that tau-dependent nuclear envelope invagination and relocalization of LInker of Nucleoskeleton and Cytoskeleton (LINC) complex components are conserved in a newly-developed neuroblastoma cell line that features doxycycline-inducible expression of a tau mutant associated with autosomal dominant frontotemporal dementia. We next determine that a Förster resonance energy transfer (FRET)-based sensor of nuclear tension responds to cytoskeletal stabilization and destabilization when expressed in neuroblastoma cells. Using this nuclear tension sensor, we find that induced expression of pathogenic tau is sufficient to decrease nuclear tension. This work provides the initial proof-of-concept evidence that pathogenic forms of tau alter nuclear tension, paving the way for the future study of altered nuclear mechanosensing in the context of tau-mediated neurodegenerative disorders.
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