Biochemical mechanisms of cross‐resistance to aryloxyphenoxypropionate and cyclohexanedione herbicides in populations of Avena spp.

Abstract

Aryloxyphenoxypropionate (APP) and cyclohexanedione (CHD) herbicides are used extensively in the UK to control grass weeds, including Avena spp. (wild‐oats). Reports of resistance to APP and CHD herbicides are a particular concern for the agricultural community. In this study, the responses of four UK Avena populations were characterized towards the APP herbicides fenoxaprop‐P‐ethyl and fluazifop‐P‐butyl, and towards the CHD herbicides cycloxydim and tralkoxydim. An A. sterilis ssp. ludoviciana population (T/41) was found to be highly resistant to fenoxaprop‐P‐ethyl and fluazifop‐P‐butyl, but did not show cross‐resistance to cycloxydim and tralkoxydim. In contrast, one A. sterilis ssp. ludoviciana (T/11) and one A. fatua population (Dorset) showed partial resistance to both APP herbicides and also showed cross‐resistance to the CHD herbicide tralkoxydim, but not to cycloxydim. Before this study, the biochemical mechanisms that confer resistance to the APP and CHD herbicides in UK Avena populations were unknown. Results from the present study show that an enhanced rate of metabolism of fenoxaprop‐P‐ethyl was found to confer resistance in the two partially resistant Avena populations (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 populations was not conferred by insensitive ACCase, and was most probably caused by enhanced metabolism. This is the first report that resistance to fenoxaprop‐P‐ethyl can be conferred by enhanced metabolism in Avena spp.