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Development ePress online publication date 1 Mar 2006
doi: 10.1242/dev.02294

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Research article

PAR3 is essential for cyst-mediated epicardial development by establishing apical cortical domains


Tomonori Hirose, Mika Karasawa, Yoshinobu Sugitani, Masayoshi Fujisawa, Kazunori Akimoto, Shigeo Ohno*, and Tetsuo Noda
* Author for correspondence (e-mail: ohnos{at}med.yokohama-cu.ac.jp)

Epithelial cysts are one of the fundamental architectures for mammalian organogenesis. Although in vitro studies using cultured epithelial cells have revealed proteins required for cyst formation, the mechanisms that orchestrate the functions of these proteins in vivo remain to be clarified. We show that the targeted disruption of the mouse Par3 gene results in midgestational embryonic lethality with defective epicardial development. The epicardium is mainly derived from epicardial cysts and essential for cardiomyocyte proliferation during cardiac morphogenesis. PAR3-deficient epicardial progenitor (EPP) cells do not form cell cysts and show defects in the establishment of apical cortical domains, but not in basolateral domains. In PAR3-deficient EPP cells, the localizations of aPKC, PAR6{beta} and ezrin to the apical cortical domains are disturbed. By contrast, ZO1 and {alpha}4/{beta}1 integrins normally localize to cell-cell junctions and basal domains, respectively. Our observations indicate that EPP cell cyst formation requires PAR3 to interpret the polarity cues from cell-cell and cell-extracellular matrix interactions so that each EPP cell establishes apical cortical domains. These results also provide a clear example of the proper organization of epithelial tissues through the regulation of individual cell polarity.
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© The Company of Biologists Ltd 2006