Fig. 11. Models for Fat and distal-to-proximal signalling. (A) Analysis of WG regulation, together with studies of tissue polarity, imply that Fat activity is modulated by the juxtaposition of cells with different levels of FJ or DS activity. Both normal expression patterns and analysis of genetic mosaics imply that at FJ expression borders, Fat is inhibited in cells with less FJ, and activated in cells with more FJ. The effects of DS are more variable, but in some cases Fat is inhibited in cells with more DS, and activated in cells with less DS. Fat functions normally to inhibit WG expression. As Dachs is required for WG, and is epistatic to Fat, the simplest genetic pathway would have Fat antagonizing Dachs activity. Fat regulates some processes via Grunge; however, it is not currently known whether these also require Dachs. (B) SD-VG specifies distal wing fate, and is regulated by Notch, WG and DPP signaling. We hypothesize that FJ acts redundantly with some other gene (X), which would also be regulated by SD-VG, and which would also act through Fat to regulate WG in the proximal wing. We further suggest that DS might be repressed by WG and DPP independently of SD-VG regulation, providing an additional input into Fat signaling. Induction of WG also appears to require NUB, and to be repressed distally.