Fig. 9. Over-expression of activated Tkv mimics coro phenotypes. (A-C) dpp;GAL4/UAS-Tkv* (A), coroex11/+; dpp;GAL4/UAS-Tkv* (B) and coroex6/+; dpp;GAL4/UAS-Tkv* (C) wing discs stained for Arm to outline the cells. Over-expression of Tkv* in the AP boundary causes cleft formation similar to that in coro- discs (Fig. 6B), although the phenotype is milder. Over-expression of Tkv* in coroex6 and coroex11 heterozygous backgrounds, however, results in the formation of a deep cleft, which is normally seen in coroex11 homozygous background (Fig. 6B). Over-expression of Tkv* in coroex6 and coroex11 homozygous backgrounds caused very high levels of lethality in early larval stages. (D,E) Adult wing blades of dpp;GAL4/UAS-Tkv* (D) and coroex11/+; dpp;GAL4/UAS-Tkv* (E) flies. Note severe notching of the wing blade in E. coroex6/+; dpp;GAL4/UAS-Tkv* also showed similar phenotypes. (F,G) dpp-GAL4/UAS-DNSyx1A (F) and coroex11/coroex11; dpp-GAL4/UAS-DNSyx1A (G) wing discs stained for Arm to outline the cells. Over-expression of DN-Syx1A in the AP boundary does not cause any significant phenotype. The severity and penetrance of cleft phenotype is enhanced when DN-Syx1A is expressed in coroex11 background. G and G' show two different levels of optical sections. coroex6 over-expressing DN-Syx1A were lethal at early-third instar larval stages and therefore we were unable to examine third instar wing discs. (H,I) dpp;GAL4/UAS-Tkv* (H), coroex11/+; dpp;GAL4/UAS-Tkv* (I) and coroex6/+; dpp;GAL4/UAS-Tkv* (J) wing discs stained for Sal. Over-expression of Tkv* causes down regulation of Sal in distant cells, which is more pronounced in the posterior cells (Lecuit and Cohen, 1998). Sal levels are severely reduced in both anterior and posterior cells when Tkv* is over-expressed in coro heterozygous backgrounds.