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Hyperosmotic stress induces rewiring of 3D chromatin interactions

Flores, J. P.; Perreault, A.; Drum, Z. A.; Xu, C.; Cruz Alonso, D.; Rashid, T.; Burgess, J. D.; Fox, G. C.; Petros, G.; Wu, Y.; Kim, H.; Quiroga-Barber, I. Y.; Sahasrabudhe, I.; Lee, Y. J.; Black, E.; Li, Y.; Demmerle, J.; Strahl, B. D.; Dowen, J. M.; Wang, G. G.; Cai, D.; Phanstiel, D. H.

2026-07-30 genomics
10.64898/2025.12.19.695003 bioRxiv
Show abstract

Cells continually face environmental stressors that challenge homeostasis, yet how three-dimensional (3D) chromatin structure contributes to these stress responses remains unclear under hyperosmotic conditions. To investigate this, we map 3D chromatin structure, its molecular drivers, and transcriptional outcomes during sorbitol-induced hyperosmotic stress. Within 1 hour of sorbitol treatment, pre-existing loops and domains collapse, while several hundred de novo sorbitol-induced loops emerge. These loops are punctate, longer-range, and transient. 3D chromatin structure largely returns to baseline conditions by 24 hours. Loop reorganization is consistent across cell types and hyperosmotic stimuli. Sorbitol-induced loops require cohesin but not CTCF, and anchors are enriched at active promoters harboring GC-rich transcription factor motifs. Genes at these anchors show delayed activation following loop formation, consistent with loops acting upstream of transcription. Together, hyperosmotic stress triggers rapid, reversible, CTCF-independent chromatin reorganization that correlates with transcriptional adaptation.

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