ArticleThe Journal of cell biology2026
E- and N-cadherin drive hepatic polarity and lumen elongation via opposing effects on RhoA activity.
Article in The Journal of cell biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Hepatocytes display a unique polarity, forming narrow apical tubes-bile canaliculi (BCs)-between adjacent cells that are essential for liver function. Unlike most epithelial cells, hepatocytes express both E- and N-cadherin, yet their specific roles during BC tubulogenesis remain incompletely understood. Here, we show that these cadherins are collectively required for hepatic polarity and BC formation yet act through distinct mechanisms. E-cadherin localizes to adherens junctions, lateral membranes, and the cleavage furrow, where it promotes division-linked BC elongation and cell-cell contact formation by controlling spindle orientation and RhoA activation via NuMA and ARHGEF17. In contrast, N-cadherin is restricted to adherens junctions and maintains hepatic polarity by attenuating RhoA activity through the p120-catenin family member ARVCF and its partner p190B/ARHGAP5. Together, these findings reveal that dual cadherin expression drives hepatic polarity and BC formation by controlling RhoA activity in a coordinated yet opposing manner.
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