TY - JOUR T1 - Apico-basal cell compression regulates Lamin A/C levels in Epithelial tissues JF - bioRxiv DO - 10.1101/2020.05.18.102509 SP - 2020.05.18.102509 AU - K Venkatesan Iyer AU - Natalie A. Dye AU - Suzanne Eaton AU - Frank Jülicher Y1 - 2020/01/01 UR - http://biorxiv.org/content/early/2020/05/19/2020.05.18.102509.abstract N2 - Nuclear lamina bridges mechanical forces from the cytoskeleton to the nucleus, to initiate nuclear mechanotransduction. The concentration of nuclear Lamin proteins, particularly Lamin A/C is crucial for the mechanical properties of the nucleus and nuclear mechanotransduction. Recent studies in mesenchymal tissues show that the concentration of Lamin A/C scales with stiffness and concentration of the underlying extracellular matrix (ECM). But in epithelial tissues, that lack a strong cell-ECM interaction, it is still unclear how Lamin A/C is regulated. Here, we show that concentration of Lamin A/C in epithelial tissues scales with apico-basal compression of cells and is independent of ECM concentration. But, ectopically altering the concentration of Lamin A/C does not influence cell shapes in epithelial tissues. Using genetic perturbations in Drosophila epithelial tissues, we reveal that apico-basal cell compression regulates the concentration of Lamin A/C by deforming the nucleus. We observe a similar mechanism of Lamin A/C regulation in mammalian Madin Darby Canine Kidney (MDCK) cells suggesting that this mechanism is evolutionarily conserved. Taken together, our results reveal a unidirectional mechanical coupling between cell mechanics and nuclear mechanics via the regulation of Lamin A/C. We anticipate that mechanism of Lamin A/C regulation that we revealed, could form the basis for understanding nuclear mechanotransduction in epithelial tissues.Competing Interest StatementThe authors have declared no competing interest. ER -