Mode of Action of Herbicides Affecting Acetyl-CoA Carboxylase and Fatty Acid Biosynthesis

Abstract

The mode of action of cyclohexane-l,3-dione-type (cycloxydim, clethodim, sethoxydim, tralkoxydim) and aryloxyphenoxypropanoate-type herbicides (diclofop, fenoxaprop, haloxyfop, fluazifop) is summarized in this review. Both herbicide classes, though structurally completely different, specifically block the same target enzyme i.e. the plastid acetyl-CoA carboxylase (ACC) (EC 6.4.1.2). Most members of the Poaceae are sensitive towards both herbicide groups, whereas other monocotyledonous plants as well as the dicotyledonous plants appear to be resistant. This resistance, which can be found on the level of whole plants, in isolated chloroplasts and also on the level of ACC-enzyme preparations, is apparently due to a modification of the target enzyme ACC. Within the sensitive grass family some members (Festuca and Poa species) are partially tolerant against both graminicide groups. In the case of cyclohexanedione herbicides the tolerance seems to be due to a reduced sensitivity of the target enzyme. In the case of aryloxyphenoxypropionic acid herbicides the tolerance is apparently based on a combined action of cytoplasmic factors (metabolization?) and a slightly reduced sensitivity of the target enzyme. From differences in the sensitivity of certain grasses against the two herbicide classes it is concluded that both graminicide groups bind to the same binding domaine of the ACC enzyme but possess different subsites. The consequences of the block of de novo fatty acid biosynthesis in the plastids of sensitive plants is the lack of glycerolipid and biomembrane formation which finally causes cell death in the meristematic tissues.