Survey of ACCase and ALS resistance in winter annual grasses identifies target‐site and nontarget‐site imazamox resistance in Secale cereale

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.

Characterization of imazamox-resistant shattercane (Sorghum bicolor L.) populations from Kansas

“…Enhanced metabolism of ALS-inhibiting herbicides via CYP450 enzymes has been previously reported in various grass weed species, including annual ryegrass ( Lolium rigidum Gaudin), barnyard grass ( Echinochloa crus-galli ), downy brome ( Bomu tectorum L.), and smallflower umbrella-sedge ( Cyperus difformis ) (Heap 2023; Park et al 2004; Torra et al 2021; Yu and Powles 2014). Imazamox resistance due to enhanced metabolism was recently reported in feral rye ( Secale cereale L.) (Soni et al 2022). Nevertheless, these findings can play a crucial role in developing effective, alternative management strategies, to control IMI-R populations and prevent the further evolution of imazamox resistance in shattercane populations in the region.…”

“…These pathways are regulated by enzymes that include cytochrome P450 (CYP450) monooxygenase, glycosyl transferase, and glutathione S -transferase enzymes (Yu and Powles 2014). The role of CYP450 monooxygenase enzymes in metabolic detoxification of ALS-inhibiting herbicides have been reported (Jugulam and Shyam 2019; Soni et al 2022). Malathion is an organophosphate insecticide that inhibits the activity of CYP450 monooxygenases and can indirectly elucidate the role of these enzymes in metabolic herbicide resistance (Yu and Powles 2014).…”

“…Two major mechanisms, target-site resistance (TSR) and nontarget-site resistance (NTSR), have been reported in several ALS-inhibitor-resistant weed species (Murphy and Tranel 2019; Soni et al 2022). The TSR mechanisms involve single or multiple point mutations that lead to a change in the binding affinity between the ALS inhibitor and its target enzyme (Murphy and Tranel 2019), while NTSR mechanisms involve pathways that reduce the amount of the herbicide reaching the target enzyme, including limited or reduced absorption and cellular transport, organelle sequestration, or detoxification by an enhanced metabolism (Jugulam and Shyam 2019; Soni et al 2022; Yu and Powles 2014). The NTSR mechanisms for ALS herbicides are primarily related to metabolic detoxification pathways (Jugulam and Shyam 2019; Soni et al 2022).…”

“…The TSR mechanisms involve single or multiple point mutations that lead to a change in the binding affinity between the ALS inhibitor and its target enzyme (Murphy and Tranel 2019), while NTSR mechanisms involve pathways that reduce the amount of the herbicide reaching the target enzyme, including limited or reduced absorption and cellular transport, organelle sequestration, or detoxification by an enhanced metabolism (Jugulam and Shyam 2019; Soni et al 2022; Yu and Powles 2014). The NTSR mechanisms for ALS herbicides are primarily related to metabolic detoxification pathways (Jugulam and Shyam 2019; Soni et al 2022). These pathways are regulated by enzymes that include cytochrome P450 (CYP450) monooxygenase, glycosyl transferase, and glutathione S -transferase enzymes (Yu and Powles 2014).…”

Prevalence, spatial structure and evolution of resistance to acetolactate‐synthase (ALS) inhibitors and 2,4‐D in the major weed Papaver rhoeas (L.) assessed using a massive, country‐wide sampling

“…1,2 In addition, when specific resistance mechanisms are identified, large-scale surveys are of great value in understanding their evolution and spread within and between bio-aggressor populations under the selective pressure of pesticide applications, which in turn aids resistance management. The value of such surveys has long been recognised in weed science, and largescale surveys with massive sampling have been carried out in America and especially in Australia (e.g., [3][4][5][6][7][8][9] ). Lessons from the Australian survey experience have recently been outlined.…”