<p>Two independent lines of UAS-Lef1 and UAS-Lef1-C-clamp with similar expression levels (see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1004133#pgen.1004133.s005" target="_blank">Figure S5B</a>) were assayed. Expression of either transgene with the <i>C96-Gal4</i> driver had little or no effect on wing development in an otherwise wild-type background. Percentages tabulated for the wing phenotypes seen upon knock down of TCF. Depletion of TCF/Pan with a UAS-driven RNAi hairpin causes mostly large notches, and leads to more than 20 ectopic bristles per wing and a high penetrance of L5 vein defects. Expression of human Lef1 (Lef1) significantly rescues the ectopic bristles, but has little effect on the size and frequency of the wing notches. In contrast, expression of Lef1 with the C-clamp of TCF/Pan (Lef1-C-clamp) rescues both ectopic bristles and the wing notch phenotype. (n) represents the number of wings examined for each genotype. Depletion of TCF/Pan and expression of Lef1 and Lef1-C-clamp also resulted in a disruption of the L5 vein (see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1004133#pgen-1004133-g007" target="_blank">Figure 7M</a> and data not shown). Since this phenotype has not been linked to Wg signaling, it is not considered further in this report.</p
