A precise structural organization of epithelial cells is needed for the proper functioning and development of different tissues. The epithelial cell packing mechanism is associated with mechanical interactions between cells that place the tissue in a state with the lowest free energy. In addition, planar cell polarity has been recognized as another important mechanism for the epithelial organization that ensures the orientational ordering of the cells. Planar cell polarity is a consequence of an asymmetric distribution of certain transmembrane proteins, which is driven by specific intracellular signaling pathways. Mutations and other disruptions of these pathways were found to cause an impaired cytoarchitecture of the epithelium layer. Mutant cells with disrupted activities of signaling proteins basically represent topological defects in the polarization patterns of adjacent cells, which can lead to dysfunctions in tissue operation. Motivated by the fact that regional variations of bond tensions were found in the vicinity of mutant cells, we implement a computational model that combines the tissue development processes following the concept of free energy minimization and the cellular polarization. Our results reveal that a decrease in mechanical interactions between normal and mutant epithelium cells represents a conceivable regulatory mechanism that diminishes the impact of topological defects caused by mutant cells.

上皮细胞的精确结构组织对于不同组织的正常功能和发育是必需的。上皮细胞堆积机制与使组织处于具有最低自由能状态的细胞之间的机械相互作用有关。另外，平面细胞极性被认为是确保细胞定向排列的上皮组织的另一重要机制。平面细胞极性是某些跨膜蛋白不对称分布的结果，这是由特定的细胞内信号传导途径驱动的。发现这些途径的突变和其他破坏会导致上皮层的细胞结构受损。具有信号传导蛋白活性被破坏的突变细胞基本上代表相邻细胞的极化模式中的拓扑缺陷，这可能导致组织运作的功能障碍。受在突变细胞附近发现键张力的区域变化这一事实的启发，我们实现了一种计算模型，该模型结合了遵循自由能最小化和细胞极化的概念的组织发育过程。我们的研究结果表明正常和突变上皮细胞之间的机械相互作用的减少代表了一种可能的调节机制，该机制减少了突变细胞引起的拓扑缺陷的影响。受在突变细胞附近发现键张力的区域变化这一事实的启发，我们实现了一种计算模型，该模型结合了遵循自由能最小化和细胞极化的概念的组织发育过程。我们的研究结果表明正常和突变上皮细胞之间的机械相互作用的减少代表了一种可能的调节机制，该机制减少了突变细胞引起的拓扑缺陷的影响。受在突变细胞附近发现键张力的区域变化这一事实的启发，我们实现了一种计算模型，该模型结合了遵循自由能最小化和细胞极化的概念的组织发育过程。我们的研究结果表明正常和突变上皮细胞之间的机械相互作用的减少代表了一种可能的调节机制，该机制减少了突变细胞引起的拓扑缺陷的影响。