Membrane lipids change an ion channel’s sensitivity with concentration
A bacterial channel in artificial membranes responded differently as the concentration of surrounding lipids changed. A peer-reviewed study separated the amount of activating signal needed from the maximum ion flow. Phosphatidic acid altered both, with a distinctive low-concentration response. Structural images examined closed channels under different conditions; the mechanism has not been established in human cells.
Science··Midday
Sensitivity changes before maximum flow
A membrane lipid altered how readily a bacterial ion channel responded to its activating molecule. The peer-reviewed experiment used SthK, a channel from the bacterium Spirochaeta thermophila, in artificial membrane vesicles. Phosphatidic acid at low concentrations increased sensitivity to cyclic adenosine monophosphate, or cAMP. The response approached saturation, while maximum ion transport continued to change across a wider concentration range. Lipid alone did not replace the activating molecule.[1]
Two lipids produce different patterns
Phosphatidylethanolamine, the other lipid examined, lacked the same low-concentration pattern. Across the tested range, the largest flux increased roughly 4-fold with this lipid and roughly 10-fold with phosphatidic acid. The researchers monitored ion movement using fluorescence from the vesicles’ contents. Measurements drew on at least 3 separately purified protein preparations. Changes in sensitivity and transport capacity could therefore be considered as separate functional properties.[1]
Images show closed-channel movements
Cryo-electron microscopy revealed broader movement in intracellular parts of closed channels with phosphatidic acid. Structural imaging used high lipid fractions, however, rather than directly capturing the low-concentration functional response under matching conditions. The authors also compared equally sized particle groups to examine a possible sampling effect. Their result concerns a purified bacterial model. Regulation of related channels in human heart or nerve cells was outside the demonstrated experiment.[1]
