Evidence Against a Direct Membrane Effect in the Mechanism of Action of Graminicides

Abstract

The aryloxyphenoxypropionate and cyclohexanedione herbicides, which inhibit acetyl-coenzyme A carboxylase (EC 6.4.1.2), have also been hypothesized to act at specific sites on the plasmalemma. An impermeant sulfhydryl binding agent was reported to block the diclofop acid-induced depolarization of the membrane potential (Em) in rigid ryegrass. A correlation between the antagonistic interaction with auxin herbicides both in the field and in the Emresponse, and the repolarization of Emin herbicide-resistant rigid ryegrass following removal of diclofop acid also provide support for this hypothesis. However, similar membrane responses in resistant grasses and broadleaf species suggest that the membrane response may not be important in the phytotoxic activity of the postemergence graminicides under field conditions. In addition, an antagonistic interaction was not observed in roots of susceptible grasses exposed to combinations of diclofop-methyl and 2,4-D. Furthermore, the repolarization of the Emin diclofop-resistant rigid ryegrass was correlated to differential acidification of the external solution and an increase in the protonated form of diclofop acid, rather than a site-specific interaction at the plasmalemma. Although the membrane response is probably not involved in herbicide phytotoxicity in agricultural systems, a higher extracellular pH in the resistant biotypes of rigid ryegrass may inhibit the movement of these weak-acid herbicides across the plasmalemma, and possibly contribute to increased herbicide tolerance.