This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Lucas, W. J. Articles by Wright, J. P. Search for Related Content PubMed PubMed Citation Articles by Lucas, W. J. Articles by Wright, J. P. Agricola Articles by Lucas, W. J. Articles by Wright, J. P.

Articles

Perturbation of Chara Plasmalemma Transport Function by 2[4(2',4'-Dichlorophenoxy)phenoxy]propionic Acid ¹

Department of Botany, University of California, Davis, California 95616, Metabolism and Radiation Research Laboratory United States Department of Agriculture, Science and Education Administration, Agricultural Research Service, North Dakota State University, Fargo, North Dakota 58105, Botany Department, North Dakota State University, Fargo, North Dakota 58105

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 HPO₄^–2 were still sensitive to diclofop. Currents associated with OH^– efflux and HCO₃^– 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 HCO₃^– transport by perturbing the control processes that integrate the two, without a reduction in ATP concentration.