Discovering the mechanism of enhanced metabolism in flufenacet resistant grass weeds

Inhibitors of very long chain fatty acid synthesis (VLCFAs, HRAC group K3) including flufenacet-based products are key herbicides in weed management strategies in particular of Western European cereal growing areas. They offer an alternative mode of action to those of frequently applied post-emergence active ingredients e.g. ACCase and ALS chemistries. In comparison, herbicide resistance to VLCFAs inhibitors develops considerably slower. Yet, resistance to the ‘low-risk’ herbicide flufenacet was documented in multi-resistant ryegrass (Lolium spp.) in the northwestern United States. A 46-fold resistance shift in a population from Washington State was observed in a dose-response bioassay. The resistance levels described in black-grass (Alopecurus myosuroides Huds.) field populations are lower and generally within the range of environmentally caused inconsistency in efficacy. An artificial selection of two UK multi-resistant black-grass populations with flufenacet applied annually for eight successive years resulted in resistant progeny surviving the field rate. Besides characterizing the degree of resistance in black-grass and ryegrass populations, we demonstrated that flufenacet resistance in these populations was caused by enhanced metabolism. No cross-resistance between flufenacet and pyroxasulfone, the newest VLCFAs-inhibiting herbicide, occurred in the ryegrass population. A good understanding of the resistance mechanism and early diagnostics can help preserve the efficacy of flufenacet.