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Perturbation of Chara Plasmalemma Transport Function by 2[4(2′,4′-Dichlorophenoxy)phenoxy]propionic Acid
Author(s) -
William J. Lucas,
Clyde Wilson,
John Paul Wright
Publication year - 1984
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.74.1.61
Subject(s) - depolarization , membrane potential , hyperpolarization (physics) , biophysics , chemistry , chara , dcmu , membrane transport , electrophysiology , molar concentration , reversal potential , efflux , membrane , biochemistry , stereochemistry , biology , chloroplast , patch clamp , botany , nuclear magnetic resonance spectroscopy , organic chemistry , neuroscience , gene , receptor
Electrophysiological measurements on internodal cells of Chara corallina Klein ex Willd., em. R.D.W. revealed that in the presence of (2-[4-(2',4'-dichlorophenoxy)phenoxy]propionic acid) (diclofop) the membrane potential was very sensitive to the pH of the bathing medium. At pH 5.7, 100 micromolar diclofop caused a slow reduction in the electrogenic component of the membrane potential to the value of -123 +/- 5 millivolts. Membrane resistance initially decreased, recovered transiently, then stabilized at approximately 65% of the control value. At pH 7.0, the potential appeared to plateau around -200 millivolts before rapidly declining to -140 +/- 4 millivolts; removal of diclofop resulted in recovery of the electrogenic component. Diclofop reduced cytoplasmic ATP levels by 96.4% and 36.6% at pH 5.7 and 7.0, respectively. At pH 8.2, diclofop did not change the ATP concentration significantly, but induced a hyperpolarization of the membrane potential to near -250 millivolts, and also reduced or inhibited the dark-induced hyperpolarization; the light-induced depolarization was reduced to a lesser extent. DCMU applied in the light elicited the same response at the plasmalemma as placing cells in the dark. When K(+) channels were opened and cells depolarized with 10 millimolar K(+), diclofop induced a further depolarization of approximately 30 millivolts. Cells decoupled with HPO(4) (-2) were still sensitive to diclofop. Currents associated with OH(-) efflux and HCO(3) (-) influx, as measured with a vibrating probe technique, became spatially destabilized and reduced in magnitude in the presence of diclofop. After 60 minutes, most of the cell surface was engaged in a low level of OH(-) efflux activity. The results indicate that diclofop may be a proton ionophore at pH 7.0 and 5.7. At pH 8.2, diclofop may inhibit the operation of the H(+)-ATPase and OH(-) efflux systems associated with HCO(3) (-) transport by perturbing the control processes that integrate the two, without a reduction in ATP concentration.

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