Models for cytokinesis-linked hepatocyte polarization and BC formation. (A) Schematic illustrating the overlapping and distinct roles of E-cadherin and N-cadherin in controlling BC elongation and maintaining hepatic polarity via opposing effects on RhoA activity. E-cadherin activates RhoA at the AJs surrounding the BC and at the cleavage furrow via ARHGEF17, while restricting active RhoA to the division site via NuMA at the lateral membrane during cytokinesis. This spatially restricted RhoA activity enables the recruitment of E-cadherin to nascent cell–cell contacts between daughter cells, promoting new AJ assembly during primordial BC formation and BC elongation. ARHGEF17 and NuMA also contribute to BC elongation by regulating spindle orientation (see below). While N-cadherin shares the role of promoting AJ assembly during primordial BC formation with E-cadherin, it also decreases RhoA activity at AJs via ARVCF and p190B RhoGAP, thereby preventing an unwanted switch from hepatic to columnar polarity. (B) Model depicting the roles of two distinct mechanical forces in regulating spindle orientation during BC elongation. The first force is generated by E-cadherin–NuMA–dynein–astral MT pathway at the cell poles (#1), which governs the initial selection of spindle orientation. The second force arises from a RhoA-mediated actomyosin belt at the AJs surrounding the BC membrane, activated by ARHGEF17 (#2). This force stabilizes spindle orientation by anchoring the dividing cell at the BC side of its cleavage furrow and also provides an asymmetric mechanical cue that biases furrow ingression toward the BC (#3 and red arrow). RhoA-ROCK-dependent roles during and after contractile ring constriction enable E-cadherin delivery and/or stabilization at the division site during cytokinesis, thereby promoting nascent AJ assembly between daughter cells and driving BC elongation (#4).