1. Par1b induces asymmetric inheritance of plasma membrane domains via LGN-dependent mitotic spindle orientation in proliferating hepatocytes.
- Author
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Slim CL, Lázaro-Diéguez F, Bijlard M, Toussaint MJ, de Bruin A, Du Q, Müsch A, and van Ijzendoorn SC
- Subjects
- Cell Proliferation, Hep G2 Cells physiology, Humans, Cell Membrane physiology, Cell Polarity physiology, Hepatocytes physiology, Intracellular Signaling Peptides and Proteins physiology, Metalloproteases physiology, Mitochondrial Proteins physiology, Spindle Apparatus physiology
- Abstract
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 non-polarized 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., Competing Interests: The authors have declared that no competing interests exist.
- Published
- 2013
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