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1 May 2004 A role for glutathione S-transferases in resistance to herbicides in grasses
John P. H. Reade, Lucy J. Milner, Andrew H. Cobb
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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.

Nomenclature: Blackgrass, Alopecurus myosuroides Huds. ALOMY.

John P. H. Reade, Lucy J. Milner, and Andrew H. Cobb "A role for glutathione S-transferases in resistance to herbicides in grasses," Weed Science 52(3), 468-474, (1 May 2004).
Received: 1 November 2002; Accepted: 1 April 2003; Published: 1 May 2004
cytochrome P450
metabolism-based resistance
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