Sawada Yasuyuki, Sokabe Masahiro
Department of Physiology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan.
Eur Biophys J. 2015 Oct;44(7):531-43. doi: 10.1007/s00249-015-1065-2. Epub 2015 Aug 2.
One of the goals of mechanosensitive channel (MSC) studies is to understand the underlying molecular and biophysical mechanisms of the mechano-gating process from force sensing to gate opening. We focus on the latter process and investigate the role of water in the bacterial MSC MscL, which is activated by membrane tension. We analyze the interplay between water and the gate-constituting amino acids, Leu19-Gly26, through molecular dynamics simulations. To highlight the role of water, specifically hydration of the gate, in MscL gating, we restrain lateral movements of the water molecules along the water-vapor interfaces at the top and bottom of the vapor bubble, plugging the closed gate. The gating behaviors in this model and the normal MscL model, in which water movements are unrestrained, are compared. In the normal model, increased membrane tension breaks the hydrogen bond between Leu19 and Val 23 of the inner helix, exposing the backbone carbonyl oxygen of Leu19 to the water-accessible lumen side of the gate. Associated with this activity, water comes to access the vapor region and stably interacts with the carbonyl oxygen to induce a dewetting to wetting transition that facilitates gate expansion toward channel opening. By contrast, in the water-restrained model, carbonyl oxygen is also exposed, but no further conformational changes occur at the gate. This suggests that gate opening relies on a conformational change initiated by wetting. The penetrated water weakens the hydrophobic interaction between neighboring transmembrane inner helices called the "hydrophobic lock" by wedging into the space between their interacting portions.
机械敏感通道(MSC)研究的目标之一是了解从力感知到门控开放的机械门控过程的潜在分子和生物物理机制。我们专注于后一个过程,并研究水在细菌MSC MscL中的作用,MscL由膜张力激活。我们通过分子动力学模拟分析水与构成门的氨基酸Leu19 - Gly26之间的相互作用。为了突出水,特别是门的水合作用在MscL门控中的作用,我们限制水分子在蒸汽泡顶部和底部沿水 - 气界面的横向运动,堵塞关闭的门。比较了该模型与水运动不受限制的正常MscL模型中的门控行为。在正常模型中,增加的膜张力打破了内螺旋的Leu19和Val 23之间的氢键,使Leu19的主链羰基氧暴露于门的水可及内腔侧。伴随着这种活动,水进入蒸汽区域并与羰基氧稳定相互作用,引发从去湿到湿润的转变,促进门向通道开放的扩展。相比之下,在水限制模型中,羰基氧也会暴露,但门处不会发生进一步的构象变化。这表明门的开放依赖于由湿润引发的构象变化。渗透的水通过楔入相邻跨膜内螺旋相互作用部分之间的空间,削弱了称为“疏水锁”的相邻跨膜内螺旋之间的疏水相互作用。