ArticleScience advances2025
ATR-hippo drives force signaling to nuclear F-actin and links mechanotransduction to neurological disorders.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- The responsive nucleus: morphological signatures of cellular state.Nucleus (Austin, Tex.) · 2026Review
- Cancer drug response and resistance: molecular mechanisms and combating strategies.Signal transduction and targeted therapy · 2026Review
- Structural Remodeling of TCR-HLA-DQ8 Recognition by a β-Cell Stress-Associated C19S Insulin Neoepitope in Type 1 Diabetes.International journal of molecular sciences · 2026Article
- Roles of DNA Damage Response Pathway in the Regulation of the Nuclear Envelope.Current issues in molecular biology · 2026Review
- Nuclear rupture in confined cell migration triggers nuclear actin polymerization to limit chromatin leakage.The EMBO journal · 2025Article
Corrections and comments
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Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanical environment is sensed through cell-matrix contacts with the cytoskeleton, but how signals transit the nuclear envelope to affect cell fate decisions remains unknown. Nuclear actin coordinates chromatin motility during differentiation and genome maintenance, yet it remains unclear how nuclear actin responds to mechanical force. The DNA-damage kinase ataxia telangiectasia and Rad3-related protein (ATR) translocates to the nuclear envelope to protect the nucleus during cell motility or compression. Here, we show that ATR drives nuclear actin assembly via recruitment of Filamin-A to the inner nuclear membrane through binding of the hippo pathway scaffold and ATR substrate, RASSF1A. Moreover, we demonstrate how germline RASSF1 mutation disables nuclear mechanotransduction resulting in cerebral cortex thinning and associates with common psychological traits. Thus, defective mechanical-regulated pathways may contribute to complex neurological disorders.
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Registered trials
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