Bauer R, Weimbs A, Lechner H, Hoch M
Institute of Molecular Physiology and Developmental Biology, University of Bonn, Bonn, Germany.
Cell Commun Adhes. 2006 Jan-Apr;13(1-2):103-14. doi: 10.1080/15419060600631839.
The Drosophila innexin multigene family of gap junction encoding proteins consists of eight family members whose function in epithelial morphogenesis is mostly unknown. We have recently shown that innexin2 plays a crucial role in the organization of embryonic epithelia. Innexin2 protein accumulates in the epidermis in the apico-lateral membrane domain and colocalizes with core proteins of adherens junctions, such as DE-cadherin and Armadillo, the ss -catenin homolog. Innexin2 localization is altered in both armadillo and DE-cadherin mutants Biochemical interaction studies point to a direct interaction of DE-cadherin and Armadillo with innexin2 suggesting a close link between gap junction and adherens junction biogenesis. We have used the Drosophila Schneider cell tissue culture system to further study the interaction of innexin2 with DE-cadherin. Our results provide evidence that DE-cadherin may be a key component to control trafficking, and localization of Innexin2 to the plasma membrane.
果蝇中编码间隙连接蛋白的Innexin多基因家族由八个家族成员组成，其在上皮形态发生中的功能大多未知。我们最近发现Innexin2在胚胎上皮组织的形成中起关键作用。Innexin2蛋白在表皮的顶侧膜结构域积累，并与黏着连接的核心蛋白共定位，如DE-钙黏蛋白和犰狳蛋白（β-连环蛋白的同源物）。在犰狳蛋白和DE-钙黏蛋白突变体中，Innexin2的定位发生改变。生化相互作用研究表明，DE-钙黏蛋白和犰狳蛋白与Innexin2直接相互作用，这表明间隙连接和黏着连接的生物发生之间存在密切联系。我们利用果蝇Schneider细胞组织培养系统进一步研究Innexin2与DE-钙黏蛋白的相互作用。我们的结果提供了证据，表明DE-钙黏蛋白可能是控制Innexin2运输以及其在质膜上定位的关键成分。
