Fig. 3. Gain of function in the Wingless pathway specifically increases the size of Slouch cluster II. Ventral views of late stage 11 embryos were stained with Slouch antibody; ventral views are shown and anterior is left. cI (black arrowhead) and cII (white arrowhead) are indicated in both panel and insets. Black arrows denote the midline in panels and Slouch-expressing CNS cells in the insets. Insets show one hemisegment for each condition. The effect of different levels of Wg signaling were assayed in embryos of the following genotypes: (A) wild-type, (B) twiGAL4>UASwg^E, (C) twiGAL4>UASarm^s10, (D) dAPC2^d40, (E) twiGAL4;twiGAL4>UASwg^E and (F) twiGAL4;Dmef2GAL4>UASwg^E. As shown in B-F, increased Wg signaling led to an increase in cII size (white arrowhead) to 5-15 cells, mode=12. cI size (black arrowhead) was unaffected. Four cells constitute cII in wild-type; two cells make up cI. Higher Slouch expression was detected in the visceral mesoderm in F. We detect displacement of cI towards the midline in these experiments. This effect may be due to the GAL4 drivers used to manipulate Wg signaling. (G) Quantification of cluster expansion in Wg pathway gain-of-function experiments. Graphs show percentage of hemisegments that show cluster expansion, cII (red) and cI (blue). ^**, conditions where cI was expanded from two cells; n, number of hemisegments counted. The mode number of cells increased in cII under gain-of-function conditions was 12 for each condition.