Par1b induces asymmetric inheritance of plasma membrane domains via LGN-dependent mitotic spindle orientation in proliferating hepatocytes

Slim, C. L., Lázaro-Diéguez, F., Bijlard, M., Toussaint, M. J. M., de Bruin, A., Du, Q., Müsch, A. & van Ijzendoorn, S. C. D., 17-Dec-2013, In : PLOS BIOLOGY. 11, 12, 13 p., e1001739.

Research output: Contribution to journalArticleAcademicpeer-review

  • Christiaan L Slim
  • Francisco Lázaro-Diéguez
  • Marjolein Bijlard
  • Mathilda J M Toussaint
  • Alain de Bruin
  • Quansheng Du
  • Anne Müsch
  • Sven C D van Ijzendoorn

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.

Original languageEnglish
Article numbere1001739
Number of pages13
Issue number12
Publication statusPublished - 17-Dec-2013


  • Cell Membrane, Cell Polarity, Cell Proliferation, Hep G2 Cells, Hepatocytes, Humans, Intracellular Signaling Peptides and Proteins, Metalloproteases, Mitochondrial Proteins, Spindle Apparatus

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