Par1b induces asymmetric inheritance of plasma membrane domains via LGN-dependent mitotic spindle orientation in proliferating hepatocytes.
PLoS Biol
; 11(12): e1001739, 2013 Dec.
Article
en En
| MEDLINE
| ID: mdl-24358023
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.
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Membrana Celular
/
Polaridad Celular
/
Hepatocitos
/
Proteínas Mitocondriales
/
Metaloproteasas
/
Péptidos y Proteínas de Señalización Intracelular
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Huso Acromático
Límite:
Humans
Idioma:
En
Año:
2013
Tipo del documento:
Article