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First published online 27 February 2008
doi: 10.1242/dev.015982

This Article Figures Only Full Text Full Text (PDF) Supplementary Material OA All Versions of this Article: dev.015982v1 135/7/1355    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by Shindo, M. Articles by Hayashi, S. PubMed PubMed Citation Articles by Shindo, M. Articles by Hayashi, S.

Dual function of Src in the maintenance of adherens junctions during tracheal epithelial morphogenesis

Masayo Shindo^1,2, Housei Wada¹, Masako Kaido¹, Minoru Tateno¹, Toshiro Aigaki³, Leo Tsuda^1,* and Shigeo Hayashi^1,2,4,

¹ Riken Center for Developmental Biology, 2-2-3 Minatojima-minamimachi, Chuo-ku Kobe 650-0047, Japan.
² National Institute of Genetics and the Graduate School for Advanced Studies, 1111 Yata, Mishima, Shizuoka-ken 411-8540, Japan.
³ Department of Biology, Tokyo Metropolitan University, Minami-Ohsawa 1-1, Hachioji, Tokyo 192-0397, Japan.
⁴ Department of Life Science, Kobe University Graduate School of Sciences and Technology, Kobe 657-8501, Japan.

Author for correspondence (e-mail: shayashi{at}cdb.riken.jp)

Accepted 24 January 2008

The downregulation of E-cadherin by Src promotes epithelial to mesenchymal transition and tumorigenesis. However, a simple loss of cell adhesion is not sufficient to explain the diverse developmental roles of Src and metastatic behavior of viral Src-transformed cells. Here, we studied the functions of endogenous and activated forms of Drosophila Src in the context of tracheal epithelial development, during which extensive remodeling of adherens junctions takes place. We show that Src42A is selectively activated in the adherens junctions of epithelia undergoing morphogenesis. Src42A and Src64B are required for tracheal development and to increase the rate of adherens junction turnover. The activation of Src42A caused opposing effects: it reduced the E-cadherin protein level but stimulated transcription of the E-cadherin gene through the activation of Armadillo and TCF. This TCF-dependent pathway was essential for the maintenance of E-cadherin expression and for tissue integrity under conditions of high Src activity. Our data suggest that the two opposing outcomes of Src activation on E-cadherin facilitate the efficient exchange of adherens junctions, demonstrating the key role of Src in the maintenance of epithelial integrity.

Key words: Src, E-cadherin, Armadillo, Drosophila, Trachea, Cancer

This article has been cited by other articles:

				M. Affolter and E. Caussinus Tracheal branching morphogenesis in Drosophila: new insights into cell behaviour and organ architecture Development, June 15, 2008; 135(12): 2055 - 2064. [Abstract] [Full Text] [PDF]

				M. Shindo, H. Wada, M. Kaido, M. Tateno, T. Aigaki, L. Tsuda, and S. Hayashi Dual function of Src in the maintenance of adherens junctions during tracheal epithelial morphogenesis J. Cell Sci., April 1, 2008; 121(7): e707 - e707. [Full Text]