Cases and Mechanisms of Resistance to ACCase-Inhibiting Herbicides

摘要

Aryloxyphenoxypropionate (AOPP) and cyclohexanedione (CHD) herbicides have been used widely for the control of many grass weeds since their respective introductions in the 1970s and 1980s. The target site of AOPP and CHD herbicides is the biotin-containing enzyme acetyl-coenzyme A carboxylase (EC 6.4.1.2, ACCase), which catalyzes the ATP-dependent conversion of acetyl-coenzyme A to malonyl-coenzyme A in the fatty acid biosynthetic pathway. Grass plants are sensitive to these herbicides because they contain only the herbicide-sensitive eukaryotic form of ACCase in their plastids and cytosol. Because of the frequent and widespread use of these graminicides, fourteen grass weed species have developed resistance to AOPP and CHD herbicides in several countries around the world. The predominant mechanism of weed resistance to ACCase inhibiting herbicides appears to involve alterations of the target ACCase enzyme. Alternative mechanisms such as overexpression of ACCase activity, enhanced herbicide metabolism, and reduced effects of the AOPP and CHD herbicides on the electrogenic potential of plasma membrane have been proposed to explain the development of resistance to AOPP and CHD herbicides in selected grass weeds. The mechanisms of weed resistance to ACCase inhibiting herbicides and the case of an accession of smooth crabgrass [Digitaria ischaemum (Schleb.) Muhl.], which has developed resistance to the herbicide fenoxaprop-ethyl are discussed in this chapter.