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. 2015 Jul 29;309(7):R747–R756. doi: 10.1152/ajpregu.00148.2015

Fig. 6.

Fig. 6.

Knockdown of Irk1 and Irk2 together reveals a K+ secretory defect, with no additional effect of Irk3 knockdown. A: transepithelial K+ flux (pmol/min per tubule) was measured in tubules from control flies (w;c42-GAL4/+ and w;UAS-Irk2RNAi/+;UAS-Irk1RNAi/+) or from flies in which Irk1 and Irk2 were simultaneously knocked down in the principal cells under the control of c42-GAL4 (w;UAS-Irk2RNAi/+;c42-GAL4/UAS-Irk1RNAi). K+ flux was decreased in the Irk1/Irk2 double-knockdown tubules. Flies in this experiment were reared at room temperature, ∼22–23°C; n = 41–42 tubules/genotype. *P < 0.05; ***P < 0.001. B: transepithelial K+ flux (pmol/min per tubule) was measured in tubules from control flies (w;UAS-Irk2RNAi/+;UAS-Irk1RNAi/+) or from flies in which Irk1 and Irk2 were simultaneously knocked down in the principal cells under the control of c42-GAL4 (w;UAS-Irk2RNAi/+;c42-GAL4/UAS-Irk1RNAi) or from flies in which Irk1, Irk2, and Irk3 were simultaneously knocked down (w;UAS-Irk2RNAi/+;c42-GAL4 UAS-Irk3RNAi/UAS-Irk1RNAi). K+ flux was decreased in the Irk1/Irk2 double-knockdown tubules but was not further decreased in the Irk1/Irk2/Irk3 triple-knockdown tubules. Flies in this experiment were reared at room temperature, ∼22–23°C; n = 20–22 tubules/genotype. **P < 0.01.