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首页> 外文期刊>Plant physiology >Blue light activates potassium-efflux channels in flexor cells from Samanea saman motor organs via two mechanisms
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Blue light activates potassium-efflux channels in flexor cells from Samanea saman motor organs via two mechanisms

机译：蓝光通过两种机制激活萨曼萨曼萨曼运动器官屈肌细胞的钾外流通道

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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. [References: 41]
机译：光诱导的萨摩亚萨曼小叶运动取决于运动细胞中膜转运蛋白的调节。蓝光（BL）通过诱导屈肌运动细胞释放K +刺激小叶开放。为了阐明光对K +外排（K-D）通道调节的机制，在变化的照明过程中，将屈肌运动细胞原生质体贴片固定在细胞附着的结构中。去极化通过单个开放的K-D通道引起向外的电流。通过施加电压斜坡并跟踪K-D通道电流的表观反向电位的变化来估算细胞膜电位（E-M）的变化。 BL使E-M沿正方向移动（即使电池去极化）约10 mV。随后的红光脉冲和随后的黑暗使E-M反向移动（即使细胞超极化）。在用氢泵抑制剂预处理的细胞中未观察到BL诱导的E-M转变，表明氢泵对该转变有贡献。 BL还以独立于电压的方式增加了K-D通道的活性，这反映在相对于表观反转电势（G（@ 40））去极化时，平均净稳态贴片电导的增加为40 mV。在不改变单通道电导的情况下，G（@ 40）大约增加了12 pS，这可能是通过增加通道打开的可能性引起的。随后的红光和黑暗反转了G（@ 40）的变化。因此，K +外排是屈肌细胞细胞体积减少的决定因素，由BL通过膜电位和独立的信号传导途径双重调控。 [参考：41]

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