Roy Tanusri, Ghosh Swetlana, Piplani Niyati, Sthanam Lakshmi Kavitha, Tiwary Niharika, Dhar Sayak, Konyak W Chingmei Wangsa, Panigrahi Santosh Surendra, Singh Priya, Sowpati Divya Tej, Nair Sreelaja, Kumar Sushil, Shekar P Chandra, Sen Shamik
Department of Biosciences & Bioengineering, IIT Bombay, Mumbai 400076, India.
Centre for Cellular and Molecular Biology, Hyderabad 500007, India.
Nucleic Acids Res. 2025 Sep 5;53(17). doi: 10.1093/nar/gkaf852.
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.
胚胎干细胞(ESC)易受DNA损伤影响,其存活依赖于强大且高效的DNA损伤反应(DDR)机制。然而,物理力介导的DNA损伤对ESC命运的影响仍不清楚。我们发现,小鼠胚胎干细胞(mESC)的硬度依赖性铺展通过核压缩诱导DNA损伤,DNA损伤通过核纤层蛋白A/C导致分化。有趣的是,分化与DNA损伤以及DDR因子如ATR和CHK1的激活有关。虽然通常已知ATR在DDR途径中发挥作用,但其在硬度介导的核压缩和mESC分化过程中的作用尚不清楚。虽然我们的结果显示在硬底物上CHK1途径的激活和活化的ATR在核内富集,但抑制ATR和CHK1均通过不同机制导致核纤层蛋白A/C表达降低。总体而言,我们证明mESC分化是由核压缩介导的DNA损伤驱动的,并且涉及ATR依赖性的核纤层蛋白A/C调节。