Elevation of the mechanically-sensitive e protein emerin links nuclear mechanotransduction to tau-induced cytoskeletal remodeling in neurons.
Overview
- Department of Cell Systems and Anatomy, Barshop Institute for Longevity and Aging Studies, Glenn Biggs Institute for Alzheimer’s and Neurodegenerative Diseases, University of Texas Health San Antonio, San Antonio, TX, USA
- Department of Biochemistry and Structural Biology, University of Texas Health San Antonio, San Antonio, TX, USA
- Department of Molecular Biology, Cell Biology and Biochemistry, Center for Alzheimer’s Disease Research, Brown University, Providence, RI, USA
- Greehey Children’s Cancer Research Institute, University of Texas Health San Antonio, San Antonio, TX, USA
Abstract
Neurodegenerative tauopathies, including Alzheimer’s disease, are neuropathologically defined by pathological tau deposition. While tau drives neurotoxicity by disrupting cytoskeletal, nucleoskeletal, and genomic architecture, cellular mechanisms mediating tau-induced dysfunction of the cytoskeleton and nucleoskeleton are incompletely understood. Here, we identify proteins with differing abundance in a cellular tauopathy model, iTau. Building upon previous findings that pathogenic tau reduces nuclear tension, we find elevated levels of emerin, a central regulator of nuclear mechanotransduction, in iTau neurons and tau mutant iPSC-derived neurons. Neuronal emerin overexpression drives neurotoxicity, increases filamentous actin (F-actin), and induces nuclear invagination, mimicking cellular phenotypes of tauopathy. Alterations in emerin binding partners reflect its cytosolic relocalization in iTau neurons, suggesting that pathogenic tau may impact nuclear mechanotransduction by altering emerin levels and localization. Overall, we identify emerin as a potential mediator of cytoskeletal and nucleoskeletal remodeling in tauopathy and provide a foundation for future studies of emerin function in neurons.
Reproduced under the paper's license (CC BY), from the paper cited above.
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Data
Datasets cited
- figshare:32932663, at figshare; found in DataCite
Data availability statement
Mass spectrometry datasets will be made publicly available through the ProteomeXchange upon acceptance of the manuscript.
Reproduced under the paper's license (CC BY), from the paper cited above.
Versions
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Version 1, 27 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 10 authors, 8 keywords, 10 MeSH terms, 2 funders, 65 references.
Cite
This paper
Sohn, C., Pardo, S., Molleur, D., Paduri, S. R., Lambert, M., Uttke, Z., Sohn, E. J., Thomas, M. G., Weintraub, S. T., & Frost, B. (2026). Elevation of the mechanically-sensitive e protein emerin links nuclear mechanotransduction to tau-induced cytoskeletal remodeling in neurons. Nucleus (Austin, Tex.), 17(1), 2697135. https://
BibTeX
@article{sohn2026elevati
author = {Sohn, Claira and Pardo, Sammy and Molleur, Dana and Paduri, Satvik R. and Lambert, Morgan and Uttke, Zachary and Sohn, Erich J. and Thomas, Morgan G. and Weintraub, Susan T. and Frost, Bess},
title = {{Elevation of the mechanically-sensitive e protein emerin links nuclear mechanotransduction to tau-induced cytoskeletal remodeling in neurons}},
journal = {Nucleus (Austin, Tex.)},
year = {2026},
month = jul,
volume = {17},
number = {1},
pages = {2697135},
publisher = {Taylor \& Francis},
issn = {1949-1034},
doi = {10.1080/
url = {https://
pmid = {42415348},
pmcid = {PMC13349007}
}
RIS
TY - JOUR
AU - Sohn, Claira
AU - Pardo, Sammy
AU - Molleur, Dana
AU - Paduri, Satvik R.
AU - Lambert, Morgan
AU - Uttke, Zachary
AU - Sohn, Erich J.
AU - Thomas, Morgan G.
AU - Weintraub, Susan T.
AU - Frost, Bess
TI - Elevation of the mechanically-sensitive e protein emerin links nuclear mechanotransduction to tau-induced cytoskeletal remodeling in neurons
T2 - Nucleus (Austin, Tex.)
J2 - Nucleus
PY - 2026
DA - 2026/
VL - 17
IS - 1
SP - 2697135
SN - 1949-1034
PB - Taylor & Francis
DO - 10.1080/
UR - https://
LA - en
ER -
CSL-JSON
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