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蓝光通过两种机制激活雨树运动器官屈肌细胞中的钾离子外流通道。

Blue light activates potassium-efflux channels in flexor cells from Samanea saman motor organs via two mechanisms.

作者信息

Suh S, Moran N, Lee Y

机构信息

Department of Life Science, School of Environmental Engineering, Pohang University of Science and Technology, Pohang, 790-784, Republic of Korea.

出版信息

Plant Physiol. 2000 Jul;123(3):833-43. doi: 10.1104/pp.123.3.833.

Abstract

Light-induced leaflet movement of Samanea saman depends on the regulation of membrane transporters in motor cells. Blue light (BL) stimulates leaflet opening by inducing K(+) release from the flexor motor cells. To elucidate the mechanism of K(+)-efflux (K(D))-channel regulation by light, flexor motor cell protoplasts were patch-clamped in a cell-attached configuration during varying illumination. Depolarization elicited outward currents through single open K(D) channels. Changes in cell membrane potential (E(M)) were estimated by applying voltage ramps and tracking the change of the apparent reversal potential of K(D)-channel current. BL shifted E(M) in a positive direction (i.e. depolarized the cell) by about 10 mV. Subsequent red light pulse followed by darkness shifted E(M) oppositely (i.e. hyperpolarized the cell). The BL-induced shifts of E(M) were not observed in cells pretreated with a hydrogen-pump inhibitor, suggesting a contribution by hydrogen-pump to the shift. BL also increased K(D)-channel activity in a voltage-independent manner as reflected in the increase of the mean net steady-state patch conductance at a depolarization of 40 mV relative to the apparent reversal potential (G(@40)). G(@40) increased by approximately 12 pS without a change of the single-channel conductance, possibly by increasing the probability of channel opening. Subsequent red-light and darkness reversed the change in G(@40). Thus, K(+) efflux, a determining factor for the cell-volume decrease of flexor cells, is regulated by BL in a dual manner via membrane potential and by an independent signaling pathway.

摘要

雨树叶片的光诱导运动依赖于运动细胞中膜转运蛋白的调节。蓝光(BL)通过诱导屈侧运动细胞释放钾离子来刺激叶片张开。为了阐明光对钾离子外流(K(D))通道的调节机制,在不同光照条件下,以细胞贴附模式对屈侧运动细胞原生质体进行膜片钳记录。去极化通过单个开放的K(D)通道引发外向电流。通过施加电压斜坡并跟踪K(D)通道电流的表观反转电位变化来估计细胞膜电位(E(M))的变化。蓝光使E(M)向正向移动(即细胞去极化)约10 mV。随后的红光脉冲加黑暗则使E(M)向相反方向移动(即细胞超极化)。在用氢泵抑制剂预处理的细胞中未观察到蓝光诱导的E(M)移动,这表明氢泵对这种移动有作用。蓝光还以电压非依赖的方式增加K(D)通道活性,这表现为在相对于表观反转电位去极化40 mV时平均净稳态膜片电导(G(@40))增加。G(@40)增加了约12 pS,而单通道电导没有变化,可能是通过增加通道开放的概率。随后的红光和黑暗使G(@40)的变化逆转。因此,钾离子外流是屈侧细胞体积减小的决定因素,蓝光通过膜电位和独立的信号通路以双重方式对其进行调节。

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