Figure 1.

A hypothetical 2-molecule model for KCNJ15/Kir4.2 and intracellular polyamines in electric field sensing through biased inward rectification of potassium channels. (A) In an electric field, intracellular polyamines accumulate at the cathode-facing side and modulate the rectification property of KCNJ15/Kir4.2. The cathode would show an increased inward rectifying property, whereas the anode side would show a decreased inward rectifying property. This biased inward rectification of potassium channels to the cathode side would result in directional sensing. (B) In a polyamine-depleted cell, the rectification property of KCNJ15/Kir4.2 in the cell would be lost at both cathode and anode sides thus would decrease biased inward rectification in the cell, and result in loss of directional sensing. (C) In a KCNJ15 knocked down cell, as well as in pharmacological inhibition, biased inward rectification would also be significantly decreased, causing loss of directional sensing. (D) In polyamine-binding defective mutant E157N expressing cells, polyamines cannot bind to KCNJ15/Kir4.2, so rectification property of KCNJ15/Kir4.2 in the cell would be lost at both sides, thus preventing biased inward rectification of potassium channels in an electric field resulting in loss of directional sensing.