Laitko Ulrike, Juranka Peter F, Morris Catherine E
Neuroscience OHRI and University of Ottawa, Ottawa, ON Canada K1Y 4E9.
J Gen Physiol. 2006 Jun;127(6):687-701. doi: 10.1085/jgp.200509394.
In the simplest model of channel mechanosensitivity, expanded states are favored by stretch. We showed previously that stretch accelerates voltage-dependent activation and slow inactivation in a Kv channel, but whether these transitions involve expansions is unknown. Thus, while voltage-gated channels are mechanosensitive, it is not clear whether the simplest model applies. For Kv pore opening steps, however, there is excellent evidence for concerted expansion motions. To ask how these motions respond to stretch, therefore, we have used a Kv1 mutant, Shaker ILT, in which the step immediately prior to opening is rate limiting for voltage-dependent current. Macroscopic currents were measured in oocyte patches before, during, and after stretch. Invariably, and directly counter to prediction for expansion-derived free energy, ILT current activation (which is limited by the concerted step prior to pore opening) slowed with stretch and the g(V) curve reversibly right shifted. In WTIR (wild type, inactivation removed), the g(V) (which reflects independent voltage sensor motions) is left shifted. Stretch-induced slowing of ILT activation was fully accounted for by a decreased basic forward rate, with no change of gating charge. We suggest that for the highly cooperative motions of ILT activation, stretch-induced disordering of the lipid channel interface may yield an entropy increase that dominates over any stretch facilitation of expanded states. Since tail current tau(V) reports on the opposite (closing) motions, ILT and WTIR tau(V)(tail) were determined, but the stretch responses were too complex to shed much light. Shaw is the Kv3 whose voltage sensor, introduced into Shaker, forms the chimera that ILT mimics. Since Shaw2 F335A activation was reportedly a first-order concerted transition, we thought its activation might, like ILT's, slow with stretch. However, Shaw2 F335A activation proved to be sigmoid shaped, so its rate-limiting transition was not a concerted pore-opening transition. Moreover, stretch, via an unidentified non-rate-limiting transition, augmented steady-state current in Shaw2 F335A. Since putative area expansion and compaction during ILT pore opening and closing were not the energetically consequential determinants of stretch modulation, models incorporating fine details of bilayer structural forces will probably be needed to explain how, for Kv channels, bilayer stretch slows some transitions while accelerating others.
在通道机械敏感性的最简单模型中,伸展有利于通道的扩张状态。我们之前表明,伸展可加速钾离子通道(Kv通道)中电压依赖性激活和缓慢失活,但这些转变是否涉及扩张尚不清楚。因此,虽然电压门控通道具有机械敏感性,但尚不清楚最简单的模型是否适用。然而,对于Kv通道的孔开放步骤,有充分的证据表明存在协同扩张运动。因此,为了探究这些运动如何响应伸展,我们使用了一种Kv1突变体Shaker ILT,其中在开放之前的步骤是电压依赖性电流的限速步骤。在伸展之前、期间和之后,在卵母细胞膜片上测量宏观电流。结果总是与基于扩张产生的自由能的预测相反,ILT电流激活(受孔开放之前的协同步骤限制)随着伸展而减慢,并且g(V)曲线可逆地向右移动。在WTIR(野生型,去除失活)中,g(V)(反映独立的电压传感器运动)向左移动。伸展诱导的ILT激活减慢完全是由于基本正向速率降低,门控电荷没有变化。我们认为,对于ILT激活的高度协同运动,伸展诱导的脂质通道界面无序可能导致熵增加,这超过了伸展对扩张状态的任何促进作用。由于尾电流tau(V)反映相反的(关闭)运动,我们测定了ILT和WTIR的tau(V)(尾),但其伸展响应过于复杂,难以提供太多信息。Shaw是Kv3,其电压传感器引入到Shaker中,形成了ILT模拟的嵌合体。据报道,Shaw2 F335A激活是一级协同转变,我们认为其激活可能像ILT一样随着伸展而减慢。然而,事实证明Shaw2 F335A激活呈S形,因此其限速转变不是协同的孔开放转变。此外,伸展通过一个未确定的非限速转变增加了Shaw2 F335A中的稳态电流。由于在ILT孔开放和关闭期间假定的面积扩张和压缩不是伸展调节的能量上的重要决定因素,可能需要纳入双层结构力细节的模型来解释对于Kv通道,双层伸展如何减慢一些转变而加速其他转变。