|Citation||Bauer, R., Lehmann, C., Martini, J., Eckardt, F., Hoch, M. (2004). Gap junction channel protein innexin 2 is essential for epithelial morphogenesis in the Drosophila embryo. Mol. Biol. Cell 15(6): 2992--3004. (Export to RIS)|
|Publication Type||Research paper|
|PubMed Abstract||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, immunohistochemical 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.|
What does this section display?
What does this section not display?
This section does not currently display links that were removed or gene model changes.
|All updates||Click here to see a list of all updates to this record from FB2010_08 and on.|
|Language of Publication||English|
|Additional Languages of Abstract|
|Also Published As|
|Abbreviation||Mol. Biol. Cell|
|Title||Molecular Biology of the Cell|
|Data from Reference|