Biochemical mechanisms of cross-resistance to aryloxyphenoxypropionate andcyclohexanedione herbicides in populations of Avena spp.

Aryloxyphenoxypropionate (APP) and cyclohexanedione (CHD) herbicides are us ed extensively in the UK to control grass weeds, including Avena spp. (wild -oats). Reports of resistance to APP and CHD herbicides are a particular co ncern for the agricultural community. In this study, the responses of four UK Avena populations were characterized towards the APP herbicides fenoxapr op-P-ethyl and fluazifop-P-butyl, and towards the CHD herbicides cycloxydim and tralkoxydim. An A. sterilis ssp. ludoviciana population (T/41) was fou nd to be highly resistant to fenoxaprop-P-ethyl and fluazifop-P-butyl, but did not show cross-resistance to cycloxydim and tralkoxydim. In contrast, o ne A. sterilis ssp. ludoviciana (T/11) and one A. fatua population (Dorset) showed partial resistance to both APP herbicides and also showed cross-res istance to the CHD herbicide tralkoxydim. but not to cycloxydim. Before thi s study, the biochemical mechanisms that confer resistance to the APP and C HD herbicides in UK. Avena populations were unknown. Results from the prese nt study show that an enhanced rate of metabolism of fenoxaprop-P-ethyl was found to confer resistance in the two partially resistant Avena population s (T/11 and Dorset), and the presence of an insensitive form of the target enzyme, ACCase, was responsible for target site resistance to fenoxaprop-P- ethyl and fluazifop-P-butyl in the highly resistant population T/41. Cross- resistance to the CHD herbicide tralkoxydim in the T/11 and Dorset populati ons was not conferred by insensitive ACCase, and was most probably caused b y enhanced metabolism. This is the first report that resistance to fenoxapr op-P-ethyl can be conferred by enhanced metabolism in Avena spp.