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Blue Light Activates Potassium-Efflux Channels in Flexor Cells from Samanea saman Motor Organs via Two Mechanisms
Author(s) -
SuJeong Suh,
Nava Moran,
Youngsook Lee
Publication year - 2000
Publication title -
plant physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.554
H-Index - 312
eISSN - 1532-2548
pISSN - 0032-0889
DOI - 10.1104/pp.123.3.833
Subject(s) - depolarization , membrane potential , biophysics , darkness , conductance , chemistry , reversal potential , potassium channel , patch clamp , biology , biochemistry , physics , botany , receptor , condensed matter physics
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.

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