Papazian D M, Shao X M, Seoh S A, Mock A F, Huang Y, Wainstock D H
Department of Physiology, School of Medicine, University of California, Los Angeles 90024, USA.
Neuron. 1995 Jun;14(6):1293-301. doi: 10.1016/0896-6273(95)90276-7.
The S4 segment comprises part of the voltage sensor in Shaker K+ channels. We have used a strategy similar to intragenic suppression, but without a genetic selection, to identify electrostatic interactions of the S4 segment that may be important in the mechanism of voltage-dependent activation. The S4 neutralization mutations K374Q and R377Q block maturation of the protein, suggesting that they prevent proper folding. K374Q is specifically and efficiently rescued by the second site mutations E293Q and D316N, located in putative transmembrane segments S2 and S3, respectively. These results suggest that K374, E293, and D316 form a network of strong, local, electrostatic interactions that stabilize the structure of the channel. Some other double mutant combinations result in inefficient suppression, identifying weak, presumably long-range electrostatic interactions. A simple structural hypothesis is proposed to account for the effects of the rescued double mutant combinations on the relative stabilities of open and closed channel conformations.
S4片段构成了Shaker钾离子通道中电压传感器的一部分。我们采用了一种类似于基因内抑制但无需遗传筛选的策略,来识别S4片段中可能在电压依赖性激活机制中起重要作用的静电相互作用。S4中和突变K374Q和R377Q会阻断蛋白质的成熟,这表明它们阻止了正确折叠。位于假定跨膜片段S2和S3中的第二位点突变E293Q和D316N可特异性且有效地拯救K374Q。这些结果表明,K374、E293和D316形成了一个强大的、局部的静电相互作用网络来稳定通道结构。其他一些双突变组合导致抑制效率低下,这表明存在较弱的、可能是远距离的静电相互作用。我们提出了一个简单的结构假说来解释拯救后的双突变组合对开放和关闭通道构象相对稳定性的影响。