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Establishment of cell polarity by afadin during the formation of embryoid bodies
Author(s) -
Komura Hitomi,
Ogita Hisakazu,
Ikeda Wataru,
Mizoguchi Akira,
Miyoshi Jun,
Takai Yoshimi
Publication year - 2008
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/j.1365-2443.2007.01150.x
Subject(s) - microbiology and biotechnology , nectin , adherens junction , embryoid body , biology , cdc42 , cell polarity , tight junction , embryonic stem cell , cell adhesion , actin , cell , cadherin , adult stem cell , genetics , gene
Afadin directly links nectin, an immunoglobulin‐like cell–cell adhesion molecule, to actin filaments (F‐actin) at adherens junctions (AJs). The nectin–afadin complex is important for the formation of not only AJs but also tight junctions (TJs) in epithelial cells. Studies using afadin‐knockout mice have revealed that afadin is indispensable for embryonic development by organizing the formation of cell–cell junctions. However, the molecular mechanism of cell–cell junction disorganization during embryonic development in afadin‐knockout mice is poorly understood. To address this, we took advantage of embryoid bodies (EBs) as a model system. The formation of cell–cell junctions including AJs and TJs was impaired in afadin‐null EBs. The proper accumulation of the Par complex and the activation of Cdc42 and atypical PKC (aPKC), which are crucial for the formation of cell polarity, were also inhibited by knockout of afadin. In addition, the disruption of afadin caused the abnormal deposition of laminin and the dislocalization of its receptors integrin α 6 and integrin β 1 . These results indicate that afadin organizes the formation of cell–cell junctions by regulating cell polarization in early embryonic development.