Miloshevsky Gennady V, Jordan Peter C
Department of Chemistry, Brandeis University, Waltham, Massachusetts, USA.
Biophys J. 2008 Oct;95(7):3239-51. doi: 10.1529/biophysj.108.136556. Epub 2008 Jul 11.
Potassium channels switch between closed and open conformations and selectively conduct K(+) ions. There are at least two gates. The TM2 bundle at the intracellular site is the primary gate of KcsA, and rearrangements at the selectivity filter (SF) act as the second gate. The SF blocks ion flow via an inactivation process similar to C-type inactivation of voltage-gated K(+) channels. We recently generated the open-state conformation of the KcsA channel. We found no major, possibly inactivating, structural changes in the SF associated with this massive inner-pore rearrangement, which suggests that the gates might act independently. Here we energy-minimize the open state of wild-type and mutant KcsA, validating in silico structures of energy-minimized SFs by comparison with crystallographic structures, and use these data to gain insight into how mutation, ion depletion, and K(+) to Na(+) substitution influence SF conformation. Both E71 or D80 protonations/mutations and the presence/absence of protein-buried water molecule(s) modify the H-bonding network stabilizing the P-loops, spawning numerous SF conformations. We find that the inactivated state corresponds to conformations with a partially unoccupied or an entirely empty SF. These structures, involving modifications in all four P-loops, are stabilized by H-bonds between amide H and carbonyl O atoms from adjacent P-loops, which block ion passage. The inner portions of the P-loops are more rigid than the outer parts. Changes are localized to the outer binding sites, with innermost site S4 persisting in the inactivated state. Strong binding by Na(+) locally contracts the SF around Na(+), releasing ligands that do not participate in Na(+) coordination, and occluding the permeation pathway. K(+) selectivity primarily appears to arise from the inability of the SF to completely dehydrate Na(+) ions due to basic structural differences between liquid water and the "quasi-liquid" SF matrix.
钾通道在关闭和开放构象之间转换,并选择性地传导钾离子。至少有两个门控。细胞内侧的TM2束是KcsA的主要门控,而选择性过滤器(SF)的重排则作为第二个门控。SF通过类似于电压门控钾通道C型失活的失活过程来阻断离子流。我们最近获得了KcsA通道的开放态构象。我们发现,与这种大规模的内孔重排相关的SF中没有主要的、可能导致失活的结构变化,这表明门控可能独立起作用。在此,我们对野生型和突变型KcsA的开放态进行能量最小化,通过与晶体结构比较来验证能量最小化SF的计算机模拟结构,并利用这些数据深入了解突变、离子耗尽以及钾离子与钠离子置换如何影响SF构象。E71或D80的质子化/突变以及蛋白质包埋水分子的存在与否都会改变稳定P环的氢键网络,产生众多的SF构象。我们发现失活状态对应于SF部分未占据或完全空的构象。这些结构涉及所有四个P环的修饰,通过相邻P环的酰胺氢和羰基氧原子之间的氢键得以稳定,从而阻断离子通过。P环的内部比外部更刚性。变化局限于外部结合位点,最内侧的位点S4在失活状态下持续存在。钠离子的强结合使SF在钠离子周围局部收缩,释放不参与钠离子配位的配体,并阻塞渗透途径。钾离子选择性主要似乎源于SF由于液态水和“准液态”SF基质之间的基本结构差异而无法使钠离子完全脱水。