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MBC in Press, published online ahead of print March 26, 2004
Mol. Biol. Cell 10.1091/mbc.E04-01-0056

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Submitted on January 21, 2004
Accepted on March 15, 2004

Gap junction channel protein Innexin 2 is essential for epithelial morphogenesis in the Drosophila embryo

Reinhard Bauer1, Corinna Lehmann1, Julia Martini1, Franka Eckardt1, and Michael Hoch1*

1 Institut für Molekulare Physiologie und Entwicklungsbiologie der Universität Bonn, Abt. für Molekulare Entwicklungsbiologie, Poppelsdorfer Schloss, 53115 Bonn, Germany

* Corresponding author. E-mail address: m.hoch{at}uni-bonn.de.

Direct communication of neighboring cells by gap junction channels is essential for the development of tissues and organs in the body. Whereas vertebrate gap junctions are composed of members of the connexin family of transmembrane proteins, in invertebrates gap junctions consist of Innexin channel proteins. Innexins display very low sequence homology to connexins. In addition, very little is known about their cellular role during developmental processes. In this report we examined the function and the distribution of Drosophila Innexin 2 protein in embryonic epithelia. Both loss-of-function and gain-of-function innexin 2 mutants display severe developmental defects due to cell death and a failure of proper epithelial morphogenesis. Furthermore, immunhistochemical analyses using antibodies against the Innexins 1 and 2 indicate that the distribution of Innexin gap junction proteins to specific membrane domains is regulated by tissue specific factors. Finally, biochemical interaction studies together with genetic loss- and gain-of-function experiments provide evidence that Innexin 2 interacts with core proteins of adherens and septate junctions. This is the first study, to our knowledge, of cellular distribution and protein-protein interactions of an Innexin gap junctional channel protein in the developing epithelia of Drosophila.






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