Mechanosensitive and Reversible Chromatin-Lamina Dewetting Triggers Cellular Contraction During Wound Healing
Bengoetxea, G.; Backova, L.; Arganda-Carreras, I.; Dolega, M. E.; Andreu, I.; Solon, J.
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Tissue wounding causes rapid mechanical changes in the epithelium, but how these changes affect intracellular organization remains unclear. Using the Drosophila embryonic epidermis, we show that wounding induces a fast, transient compaction of chromatin and its detachment ("dewetting") from the nuclear lamina in about half of the wound-edge cells. Within minutes, chromatin in these cells re-expands and re-associates with the lamina ("re-wetting"). This reversible chromatin-lamina dewetting is mechanosensitive, requiring both the LINC complex and intracellular calcium. During compaction, calcium is stored within chromatin and is later released during ATR-mediated expansion and lamina re-wetting. Chromatin re-expansion then triggers actomyosin contraction and promotes tissue repair through Jun kinase activation, straightening of the wound edge, and supracellular actin ring formation. Together, our findings reveal a multiscale mechanosensitive mechanism by which tissue-scale mechanical changes induce a reversible chromatin-lamina dewetting, leading to cellular contraction and initiation of tissue repair.
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