Nonmuscle myosin IIA (NMIIA) regulates anisotropic cell tension to maintain the hexagonal packing of mouse lens meridional row cells.

The mouse ocular lens is an excellent vertebrate model for epithelial cell hexagonal packing during tissue morphogenesis. As lens epithelial cells differentiate into fiber cells, the epithelial cells rearrange into hexagonally packed meridional row (MR) cells that further differentiate to form fiber cells. We previously reported that the nonmuscle myosin IIA (NMIIA)-E1841K mutation, which alters NMIIA bipolar filament assembly, significantly disrupts MR cell hexagonal packing. Immunofluorescence microscopy of MR cells demonstrates increased enrichment of NMIIA, N-cadherin, and vinculin at anterior-posterior (AP)-oriented sides of control MR cells, but equal distributions on all sides of mutant MR cells. Furthermore, F-actin is uniformly distributed around all edges of control MR cells but reduced at the AP-oriented edges of mutant MR cells. Using Bayesian Mechanical Inference, we discovered that MR cells in control lenses exhibit anisotropic junctional tension, in which relative tension is more concentrated at the AP-oriented edges. In contrast, MR cells in mutant lenses show isotropic junctional tension on all sides. We conclude that the NMIIA-E1841K mutation results in altered F-actin, NMIIA, N-cadherin, and vinculin distributions, disrupting the anisotropic orientational pattern of mechanical forces within the tissue, leading to disordered cell packing during mouse lens epithelial cell differentiation.