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Fig. 6. Src activates E-cadherin transcription through Arm. (A-C) Control; (D-F) btl>Src42A^ACT; (G,H) Src42A^myr; (I) btl>TCFN; (J,K) btl>TCFN+Src42A^ACT; (L,M) btl>wg. Tracheal cells are labeled with btl>GFP-moesin (green). (A,D,G) Arm (grayscale) is localized to the apical cell-cell junction in control embryos (A). In Src42A^ACT embryos, the Arm signal increased to fill the entire tracheal cell (D). Arm staining was reduced in Src42A mutants (G). (B,E,H,J,L) Esg expression (magenta) was localized to fusion cells in control embryos (B), and the number of Esg-expressing cells was greatly increased in embryos overexpressing Src42A^ACT or wg (E,L). In Src42A^myr or Src42A^ACT, TCFN embryos, Esg was almost undetectable (H,J). (C,F,I,K,M) shg-lacZ (nuclear signal, magenta) was broadly expressed, with elevated levels in tracheal fusion cells (C, asterisk in C'). (C'-M') Framed area in C-M enlarged and shown in grayscale. The number of strong shg-lacZ-expressing cells increased in embryos overexpressing Src42A^ACT or wg (F,M). In Src42A^myr or Src42A^ACT, TCFN embryos, shg-lacZ expression was reduced in tracheal cells (I,K; compare the levels in the trachea and ectoderm). Scale bar in A: 20 µm for A-M. (N) RNA quantification. Src42A^ACT, Src42A^GS or wg was expressed under the control of the ubiquitous da-Gal4 driver, and the levels of E-cadherin, arm and rac1 mRNAs were measured by quantitative RT-PCR. da-Gal4 embryos were used as a control.

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