ArticleNucleic acids research2025
Nuclear compression-mediated DNA damage drives ATR-dependent Lamin expression and mouse ESC differentiation.
Article in Nucleic acids research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The Underexplored Mechanobiology of Lamin A Biogenesis and Homeostasis.Biology of the cell · 2026Review
- Naïve pluripotency and genomic stability are coordinated in embryonic stem cells by a novel pluripotency regulator ZFP998.Nucleic acids research · 2026Article
- Roles of DNA Damage Response Pathway in the Regulation of the Nuclear Envelope.Current issues in molecular biology · 2026Review
- Lamin A/C facilitates DNA damage response by modulating ATM signaling and homologous recombination pathways.Animal cells and systems · 2024Article
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Authors and funding
14 authors.
Funding
Abstract
Embryonic stem cells (ESCs), which are susceptible to DNA damage, depend on a robust and highly efficient DNA damage response (DDR) mechanism for their survival. However, the implications of physical force-mediated DNA damage on ESC fate remain unclear. We show that stiffness-dependent spreading of mouse ESCs (mESCs) induces DNA damage through nuclear compression, with DNA damage causing differentiation through Lamin A/C. Interestingly, differentiation is associated with DNA damage and activation of the DDR factors such as ATR and CHK1. While ATR is typically known to play roles in DDR pathway, its role during stiffness-mediated nuclear compression and mESC differentiation is unknown. While our results show activation of CHK1 pathway and nuclear enrichment of activated ATR on stiff substrates, inhibiting ATR and CHK1 both result in reduction of Lamin A/C expression by different mechanisms. Overall, we demonstrate that mESC differentiation is driven by nuclear compression-mediated DNA damage and involves ATR-dependent modulation of Lamin A/C.
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