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. 2013 May 31;8(5):e65076. doi: 10.1371/journal.pone.0065076

Figure 5. Modulation of JAK/STAT activity phenocopies os defects.

Figure 5

(A) Dorsal hinge region of a third instar wing imaginal disc from a 10xSTATGFP, ptc>Gal4/UAS-stat92E RNAi individual showing the extent of 10xSTATGFP reporter activity (green in A, white in A’) and FasciclinIII (red in A, white in A”) to outline cell shape. P, M and D folds are labeled and the domain in which reporter activity is ablated following knockdown of stat92E is shown (arrow in A’), (B–C) Adult male flies of the indicated genotypes showing resting wing posture. Knockdown of stat92E mRNA in the ptc domain produces a clear and highly penetrant wings held out defect. (D) SEM of the dorsal wing hinge of a ptc>stat92E RNAi male with a wings held out phenotype. Compared to a wild type hinge (Figure 2A) both the first and second auxiliary sclerites (AS1 and AS2) are reduced.