Herbicide resistance is the heritable ability of a weed biotype or population to survive a herbicide application that would effectively kill a susceptible population of the weed. In the U.K. the most widespread and financially important herbicide-resistant weed is blackgrass. Investigations to elucidate the molecular mechanisms conferring herbicide resistance to blackgrass populations have been ongoing for two decades. Although the identification of target site–resistant populations has proved to be relatively straightforward (using, for example, target site assays in vitro), the study and understanding of resistance mechanisms involved in enhanced metabolism has proven to be more problematic. Research has focused on the cytochrome P450 monooxygenase and glutathione S-transferase (GST) enzyme families, both of which have been shown to be important in herbicide metabolism in many weed and crop species. GST activity and abundance are greater in a selection of herbicide-resistant blackgrass biotypes, and herbicide treatment of field populations of blackgrass results in the survival of the proportion of population possessing the greatest GST activity and abundance. In addition, GST activity in the field increases between winter and spring, and this coincides with reduced efficacy of important blackgrass herbicides. GST activities within field populations of blackgrass are highly varied, and this plasticity is discussed in relation to the development of resistant populations in field situations. This article describes research results in blackgrass and compares them with GST studies in other weed species as well as with other mechanisms for enhanced metabolism-based resistance.

Wild oat is the second-most abundant, but most economically important, weedacross the Canadian Prairies of western Canada. Despite the serious economiceffects of resistance to acetyl-CoA carboxylase (ACC) or acetolactatesynthase (ALS) inhibitors or both in this weed throughout the Northern GreatPlains of North America, little research has examined the basis forherbicide resistance. We investigated target-site and nontarget-sitemechanisms conferring ACC- and ALS-inhibitor resistance in 16 wild oatpopulations from across western Canada (four ACC-inhibitor resistant, fourALS-inhibitor resistant, and eight ACC- and ALS-inhibitor resistant). The ACC1 mutations were found in 8 of the 12 ACCinhibitor-resistant populations. The Ile1781Leu mutation was detected inthree populations, the Trp2027Cys and Asp2078Gly mutations were in twopopulations each, and the Trp1999Cys, Ile2041Asn, Cys2088Arg, and Gly2096Sersubstitutions were in one population each. Three populations had two ACC1 mutations. Only 2 of the 12 ALS inhibitor-resistantpopulations had an ALS target-site mutation—Ser653Thr andSer653Asn substitutions. This is the first global report of ALS target-site mutations in Avena spp.and four previously undocumented ACC1 mutations in wildoat. Based on these molecular analyses, seedlings of five ACC + ALSinhibitor-resistant populations (one with an ACC1 mutation;four with no ACC or ALS mutations) weretreated with malathion, a known cytochrome P450 monooxygenase inhibitor,followed by application of one of four ACC- or ALS-inhibiting herbicides.Malathion treatment often resulted in control or suppression of thesepopulations, suggesting involvement of this enzyme system in contributing toresistance to both ACC and ALS inhibitors.