Correction: Par1b Induces Asymmetric Inheritance of Plasma Membrane Domains Via LGN-Dependent Mitotic Spindle Orientation in Proliferating Hepatocytes

The development and maintenance of polarized epithelial tissue requires a tightly controlled orientation of mitotic cell division relative to the apical polarity axis.Hepatocytes display a unique polarized architecture.We demonstrate that mitotic hepatocytes asymmetrically segregate their apical plasma membrane domain to the nascent daughter cells.The nonpolarized nascent daughter cell can form a de novo apical domain with its new neighbor.This asymmetric segregation of apical domains is facilitated by a geometrically distinct ''apicolateral'' subdomain of the lateral surface present in hepatocytes.The polarity protein partitioning-defective 1/microtubule-affinity regulating kinase 2 (Par1b/MARK2) translates this positional landmark to cortical polarity by promoting the apicolateral accumulation of Leu-Gly-Asn repeat-enriched protein (LGN) and the capture of nuclear mitotic apparatus protein (NuMA)-positive astral microtubules to orientate the mitotic spindle.Proliferating hepatocytes thus display an asymmetric inheritance of their apical domains via a mechanism that involves Par1b and LGN, which we postulate serves the unique tissue architecture of the developing liver parenchyma.