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. 2012 Aug;140(2):189–205. doi: 10.1085/jgp.201210806

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© 2012 Kruse et al.

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Figure 1. — PI(4,5)P₂ depletion at the plasma membrane inhibits K_V7.x channels. (A) Currents with coexpression of K_V7.2, K_V7.3, and Dr-VSP in tsA-201 cells. The black current trace was recorded before Dr-VSP activation, the red trace was recorded 50 ms after Dr-VSP activation by a 2-s pulse to 100 mV, and the green trace was recorded 4 s after Dr-VSP activation. Test pulse protocol is shown above the traces. (B) Reduction of K_V7.2/K_V7.3-mediated tail currents by activation of Dr-VSP (n = 10). (C) Currents traces recorded from a cell expressing K_V7.1, KCNE1, Ins-5-P-FKBP-CFP, and LDR-CFP. Traces are shown before application of 5 µM rapamycin (black), after 60 s of rapamycin application (red), and after application of 100 µM XE991 (green). (D) Rapamycin-induced inhibition of XE991-sensitive current (n = 5). (E) Current trace of a cell expressing K_V7.1, KCNE1, and Dr-VSP. Currents were recorded at 10 mV, Dr-VSP was activated after 30 s with a 2-s long test pulse to 100 mV, and then the membrane potential was returned to 10 mV. At the end of the recording, XE991 was applied to determine the amount of K_V7.1-mediated current (not depicted). (F) Inhibition of XE991-sensitive current by Dr-VSP activation (n = 6). (B, D, and F) Error bars represent ±SEM.