Abstract

Electrophysiological studies in roots of pea (Pisum sativum L.) and rigid ryegrass (Lolium rigidum Gaud.) seedlings were conducted to elucidate the mechanism involved in the membrane response to the herbicide diclofop. In pea, a dicotyledonous plant insensitive to diclofop, membrane depolarization at varying pH values and herbicide concentrations increased at higher concentrations of the protonated form of diclofop acid (pKa 3.57). In unbuffered nutrient solution (pH 5.7), diclofop acid (50 [mu]M) depolarized the membrane potential (Em) in roots of both resistant and susceptible biotypes of rigid ryegrass, whereas recovery of Em occurred only in the resistant biotype following removal of the herbicide. This differential response was correlated with an increase (450%) in the rate of acidification of the external solution by the susceptible biotype, and the Em differences between biotypes were eliminated in solutions buffered at pH 5.0 or 6.0. In addition, p-chloromercuribenzene-sulfonic acid did not prevent the depolarization of Em by 50 [mu]M diclofop acid. It is concluded that the differential membrane response to diclofop acid in herbicide-resistant and -susceptible biotypes of rigid ryegrass is due to pH differences at the cell wall/plasmalemma interface. Although the membrane response is probably not involved in the primary inhibitory effect of diclofop on plant growth, it could reduce the concentration of the permeant protonated form of the herbicide and possibly could contribute to increased tolerance to diclofop and other weak acid herbicides.

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