The development of the Drosophila wing is governed by the action of two morphogens encoded by the genes decapentaplegic (dpp; a member of the BMP gene family) and wingless (wg; a member of the WNT gene family), which promote cell proliferation and pattern the wing. Along the anterior/posterior (A/P) axis, the precise expression of decapentaplegic and its receptors is required for the transcriptional regulation of specific target genes. In the present work, we analyze the function of the T-box gene optomotor-blind (omb), a decapentaplegic target gene. The wings of optomotor-blind mutants have two apparently opposite phenotypes: the central wing is severely reduced and shows massive cell death, mainly in the distal-most wing, and the lateral wing shows extra cell proliferation. Here, we present genetic evidence that optomotor-blind is required to establish the graded expression of the decapentaplegic type I receptor encoded by the gene thick veins (tkv) to repress the expression of the gene master of thick veins and also to activate the expression of spalt (sal) and vestigial (vg), two decapentaplegic target genes. optomotor-blind plays a role in wing development downstream of decapentaplegic by controlling the expression of its receptor thick veins and by mediating the activation of target genes required for the correct development of the wing. The lack of optomotor-blind produces massive cell death in its expression domain, which leads to the mis-activation of the Notch pathway and the overproliferation of lateral wing cells.
The Drosophila gene wingless encodes a secreted signalling molecule that is required for many patterning events in both embryonic and postembryonic development. In the wing wingless is expressed in a complex and dynamic pattern that is controlled by several different mechanisms. These involve the Hedgehog and Notch pathways and the nuclear proteins Pannier and U-shaped. In this report, we analyse the mechanisms that drive wingless expression in the wing hinge. We present evidence that wingless is initially activated by a secreted signal that requires the genes vestigial, rotund and nubbin. Later in development, wingless expression in the wing hinge is maintained by a different mechanism, which involves an autoregulatory loop and requires the genes homothorax and rotund. We discuss the role of wingless in patterning the wing hinge.
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