Fig. 1.

Impairment of Kinin signaling leads to tracheal air-filling defects. Tracheal air-filling defects observed upon impairment of Kinin signaling through expression of apoptosis genes (rpr, hid), inward rectifier K⁺ channel (Kir2.1), Kinin-RNAi, or ETH receptor-RNAi in Kinin neurons. Tracheal air-filling defects in flies were displayed as complete failure (black) when the tracheal system was entirely devoid of air or partial failure (gray bars). Doubling gene dosage through GAL4 expression on both second and third chromosomes [e.g., Kinin (2, 3)] caused more severe air-filling defects. Magnified image of the yellow dashed Inset box is shown Right. Arrowheads indicate the regions where failures of tracheal air-filling are observed. Larval stages examined are indicated below each bar. UAS-Kinin-RNAi and UAS-ETHR-RNAi carry UAS-Dicer2. (Scale bars, 100 μm.)