Fig. 8. Haltere-to-wing homeotic transformations induced by ectopic Vg. (A) Wild-type haltere. (B) omb-GAL4; UAS-vg haltere showing significant transformation of haltere capitellum to wing blade. Note the wing-like trichomes, which are larger, flatter and more pigmented and sparsely arranged than capitellum cells. (C) Ubx^–/Ubx⁺ halteres showing mild haltere-to-wing transformation. This is generally marked by the appearance of one or two wing-margin bristles. (D) omb-GAL4; UAS-vg/Ubx^– haltere showing enhanced homeotic transformation in a Ubx heterozygous background. The increase in the number of margin-bristles could be caused by the additive effects of increased growth, upregulated Wg signaling by overexpressed Vg and sensitized genetic (Ubx^–/+) background. This further confirms that Vg is required for the correct interpretation of Wg signaling (Klein and Martinez-Arias, 1999). (E,F) Wild-type (E) and omb-GAL4; UAS-vg- (F) haltere discs stained with anti-Salm antibodies. Salm is not normally expressed in the haltere pouch (E), nor is it induced by ectopic Vg (F). (G) Wg and Vg regulation in wing and haltere discs. Figure shows how DV signals activate Vg in non-DV cells in wing discs, and the events that are downregulated by Ubx in haltere discs. Regulatory elements of Vg are represented in two boxes: green box, vg-quadrant enhancer; white box, other enhancers of Vg that respond to Wg and probably one more, hitherto unknown, DV signal. Once activated, Vg maintains its expression by autoregulation, which is mediated through its quadrant enhancer. The discontinuous lines shown for haltere discs are the steps inhibited by Ubx during haltere specification. At the top of the hierarchy, Ubx downregulates Wg expression at the DV boundary of the posterior compartment (not shown). Although Vg-autoregulation per se is not affected, in the absence of initial activation of Vg by Wg signaling vg-QE is not activated in haltere discs.

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