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. 2017 Aug 14;114(35):E7291–E7300. doi: 10.1073/pnas.1701791114

Fig. 4.

Fig. 4.

JNK activation and tumor-like growth upon depletion of the myoblast cell population. (AF) Larval wing primordia of the indicated genotypes stained for Ci (red) and Twist (cyan; Left) and DAPI (blue) and dMMP1 (green; Right). (DF) Larvae expressed the proapoptotic gene reaper under the control of the 15B03-lexA (myo-lexA) driver. Anterior (marked as “A”) and posterior (marked as “P”) compartments are marked. hh-GAL4 drives expression to posterior cells, and Ci labels the anterior compartment. Arrows in A and D point to the endogenous expression of dMMP1 in the trachea of WT primordia. Note in B, C, E, F (Right) the ectopic expression of dMMP1 in the posterior compartment. Some background staining is observed in the folds of the anterior compartment in some discs (e.g., E). (g) Notum of a larval wing primordium expressing CD2-GFP (green) under the control of the myo-lexA driver and stained for DAPI (blue) and Twist (red). (Scale bars, AF, 50 µm; G, 30 µm.) (h) Histogram plotting the ratio between the size of the posterior (marked as “P”) compartment (labeled by the absence of Ci in AF) and the total size (marked as “T”) of wing discs of the indicated genotypes. Error bars indicate SD (n > 6 in all cases). No statistical difference (ns) in posterior compartment to total wing primordia (P/T) ratio was observed upon depletion of the myoblast population in the two tumor models [P(rod-i, p35) = 0.83, and P(Ras-V12, dlg1-i) = 0.1139].