EVIDENCE AGAINST A DIRECT MEMBRANE EFFECT IN THE MECHANISM OF ACTION OF GRAMINICIDES

The aryloxyphenoxypropionate and cyclohexanedione herbicides, which in hibit acetyl-coenzyme A carboxylase (EC 6.4.1.2), have also been hypot hesized to act at specific sites on the plasmalemma. An impermeant sul fhydryl binding agent was reported to block the diclofop acid-induced depolarization of the membrane potential (E(m)) in, rigid ryegrass. A correlation between the antagonistic interaction with auxin herbicides both in the field and in the E(m) response, and the repolarization of E(m) in herbicide-resistant rigid ryegrass following removal of diclo fop acid also provide support for this hypothesis. However, similar me mbrane responses in resistant grasses and broadleaf species suggest th at the membrane response may not be important in the phytotoxic activi ty of the postemergence graminicides under field conditions. In additi on, an antagonistic interaction was not observed in roots of susceptib le grasses exposed to combinations of diclofop-methyl and 2,4-D. Furth ermore, the repolarization of the E(m) in diclofop-resistant rigid rye grass was correlated to differential acidification of the external sol ution and an increase in the protonated form of diclofop acid, rather than a site-specific interaction at the plasmalemma. Although the memb rane response is probably not involved in herbicide phytotoxicity in a gricultural systems, a higher extracellular pH in the resistant biotyp es of rigid ryegrass may inhibit the movement of these weak-acid herbi cides across the plasmalemma, and possibly contribute to increased her bicide tolerance.