Par1b induces asymmetric inheritance of plasma membrane domains via LGN-dependent mitotic spindle orientation in proliferating hepatocytesSlim, 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 journal › Article › Academic › peer-review
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.
|Number of pages||13|
|Publication status||Published - 17-Dec-2013|
- Cell Membrane, Cell Polarity, Cell Proliferation, Hep G2 Cells, Hepatocytes, Humans, Intracellular Signaling Peptides and Proteins, Metalloproteases, Mitochondrial Proteins, Spindle Apparatus