Survey of ACCase and ALS resistance in winter annual grasses identifies target‐site and nontarget‐site imazamox resistance in Secale cereale. Issue 12 (17th September 2022)

• Record Type: Journal Article
• Authors: Soni, Neeta; Westra, Eric P.; Allegretta, Giuseppe; Araujo, André L. S.; de Pinho, Camila F.; Morran, Sarah; Lerchl, Jens; Dayan, Franck E.; Westra, Philip; Gaines, Todd A.
• Is Part Of: Pest management science. Volume 78:Issue 12(2022)
• Page Start: 5080
• Page End: 5089
• Publication Date: 2022-09-17
• Subjects: nontarget‐site resistance -- metabolic resistance -- Clearfield wheat -- cytochrome P450 -- target‐site resistance; Pests -- Control -- Periodicals; Pesticides -- Periodicals; 632.9
• DOI: 10.1002/ps.7154
• Languages: English
• ISSNs: 1526-498X

Abstract

Abstract: Background: Early detection of herbicide resistance in weeds is crucial for successful implementation of integrated weed management. We conducted a herbicide resistance survey of the winter annual grasses feral rye ( Secale cereale ), downy brome ( Bromus tectorum ), and jointed goatgrass ( Aegilops cylindrica ) from Colorado winter wheat production areas for resistance to imazamox and quizalofop. Results: All samples were susceptible to quizalofop. All downy brome and jointed goatgrass samples were susceptible to imazamox. Out of 314 field collected samples, we identified three feral rye populations (named A, B, and C) that were imazamox resistant. Populations B and C had a target‐site mechanism with mutations in the Ser653 residue of the acetolactate synthase ( ALS ) gene to Asn in B and to Thr in C. Both populations B and C had greatly reduced ALS in vitro enzyme inhibition by imazamox. ALS feral rye protein modeling showed that steric interactions induced by the amino acid substitutions at Ser653 impaired imazamox binding. Individuals from population A had no mutations in the ALS gene. The ALS enzyme from population A was equally sensitive to imazamox as to known susceptible feral rye populations. Imazamox was degraded two times faster in population A compared with a susceptible control. An oxidized imazamox metabolite formed faster in population A and this detoxification reaction was inhibited by malathion. Conclusion: Population A has a nontarget‐site mechanism of enhanced imazamox metabolism that may be conferred by cytochrome P450 enzymes. This is the first report of both target‐site and metabolism‐based imazamox resistance in feral rye. © 2022 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry. Abstract : A resistance survey in winter annual grasses identified three feral rye populations resistant to imazamox. Resistance mechanism investigations showed populations B and C contained an amino acid substitution at Ser653 in the ALS gene, whereas population A showed imazamox‐enhanced metabolism.