Appendage formation is organized by signals from discrete sources that presumably act upon downstream genes to control growth and patterning. The Drosophila vestigial gene is selectively required for wing-cell proliferation, and is sufficient to induce outgrowths of wing tissue from eyes, legs and antennae. Different signals activate separate enhancers to control vestigial expression: first, in the dorsal/ventral organizer through the Notch pathway, and subsequently, in the developing wing blade by decapentaplegic and a signal from the dorsal/ventral organizer. Signal integration must be a general feature of genes like vestigial, that regulate growth or patterning along more than one axis.
The appendages of arthropods and vertebrates possess a third, proximodistal patterning axis that is established after the primary anteroposterior and dorsoventral body axes by mechanisms that are largely unknown. The vestigial gene is required for formation of the entire Drosophila wing, and the dorsal/ventral boundary is shown to organize wing formation and vestigial gene expression. Interactions between dorsal and ventral cells in the growing imaginal disc induce vestigial gene expression through a discrete, extraordinarily conserved imaginal disc-specific enhancer. The link between dorsal/ventral compartmentalization and wing formation distinguishes the development of this sheet-like appendage from that of legs and antennae.
We present a genetic and molecular analysis of two hairy (h) pair-rule stripes in order to determine how gradients of gap proteins position adjacent stripes of gene expression in the posterior of Drosophila embryos. We have delimited regulatory sequences critical for the expression of h stripes 5 and 6 to 302 bp and 526 bp fragments, respectively, and assayed the expression of stripe-specific reporter constructs in several gap mutant backgrounds. We demonstrate that posterior stripe boundaries are established by gap protein repressors unique to each stripe: h stripe 5 is repressed by the giant (gt) protein on its posterior border and h stripe 6 is repressed by the hunchback (hb) protein on its posterior border. Interestingly, Kruppel (Kr) limits the anterior expression limits of both stripes and is the only gap gene to do so, indicating that stripes 5 and 6 may be coordinately positioned by the Kr repressor. In contrast to these very similar cases of spatial repression, stripes 5 and 6 appear to be activated by different mechanisms. Stripe 6 is critically dependent upon knirps (kni) for activation, while stripe 5 likely requires a combination of activating proteins (gap and non-gap). To begin a mechanistic understanding of stripe formation, we locate binding sites for the Kr protein in both stripe enhancers. The stripe 6 enhancer contains higher affinity Kr-binding sites than the stripe 5 enhancer, which may allow for the two stripes to be repressed at different Kr protein concentration thresholds. We also demonstrate that the kni activator binds to the stripe 6 enhancer and present evidence for a competitive mechanism of Kr repression of stripe 6.
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