Enkvetchakul Decha, Jeliazkova Iana, Nichols Colin G
Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
J Biol Chem. 2005 Oct 28;280(43):35785-8. doi: 10.1074/jbc.C500355200. Epub 2005 Sep 6.
Multiple ion channels have now been shown to be regulated by phosphatidylinositol 4,5-bisphosphate (PIP2) at the cytoplasmic face of the membrane. However, direct evidence for a specific interaction between phosphoinositides and ion channels is critically lacking. We reconstituted pure KirBac1.1 and KcsA protein into liposomes of defined composition (3:1 phosphatidylethanolamine:phosphatidylglycerol) and examined channel activity using a 86Rb+ uptake assay. We demonstrate direct modulation by PIP2 of KirBac1.1 but not KcsA activity. In marked contrast to activation of eukaryotic Kir channels by PIP2, KirBac1.1 is inhibited by PIP2 incorporated in the membrane (K(1/2) = 0.3 mol %). The dependence of inhibition on the number of phosphate groups and requirement for a lipid tail matches that for activation of eukaryotic Kir channels, suggesting a fundamentally similar interaction mechanism. The data exclude the possibility of indirect modulation via cytoskeletal or other intermediary elements and establish a direct interaction of the channel with PIP2 in the membrane.
现已证明,多种离子通道在细胞膜的胞质面受磷脂酰肌醇4,5 - 二磷酸(PIP2)调控。然而,磷酸肌醇与离子通道之间特异性相互作用的直接证据严重缺乏。我们将纯的KirBac1.1和KcsA蛋白重组到特定组成(磷脂酰乙醇胺:磷脂酰甘油为3:1)的脂质体中,并使用86Rb +摄取试验检测通道活性。我们证明PIP2可直接调节KirBac1.1的活性,但对KcsA活性无此作用。与PIP2对真核生物Kir通道的激活作用形成显著对比的是,掺入膜中的PIP2会抑制KirBac1.1(半数抑制浓度K(1/2) = 0.3 mol %)。抑制作用对磷酸基团数量的依赖性以及对脂质尾部的需求与真核生物Kir通道的激活情况相符,这表明两者存在基本相似的相互作用机制。这些数据排除了通过细胞骨架或其他中间元件进行间接调节的可能性,并证实了通道与膜中PIP2的直接相互作用。