Sourgrass (Digitaria insularis L.) and fleabane (Conyza spp. L.) constitute a major challenge to weed management in soybean [Glycine max (L.) Merr.] production systems in Brazil, especially when both are resistant to glyphosate and present concurrently. The aim of this study was to evaluate the interaction of haloxyfop-P-methyl [methyl(R)-2{4-{3-chloro-5(trifluoromethyl)-2-pyridyloxy] phenoxy} propanoate] and 2,4-D [2,4-Dichlorophenoxyacetic acid-N-methylmethanamine] to control sourgrass at three to four tillers and flowering stages and 12-to 15-cm fleabane at vegetative stage. The experiments were arranged in a randomized complete block design with four replicates and were conducted twice. Treatments were composed of haloxyfop-P-methyl and 2,4-D applied sequentially at 3-, 6-, and 12-d intervals.Treatments also included an untreated check, haloxyfop-P-methyl, and 2,4-D sequentially (without interval) and stand-alone applications of both herbicides. All treatments across experiments completely controlled fleabane plants, except haloxyfop-P-methyl alone. Haloxyfop-P-methyl applied ≥6 d before 2,4-D controlled flowering and three-to four-tiller sourgrass plants at rates of 50 and 100%, respectively. Based on results of this study, haloxyfop-P-methyl should be applied ≥6 d before 2,4-D in a sequential application structure to control fleabane and sourgrass (three or four tillers) when present concurrently.

In this work, we evaluated the short time-induced oxidative stress-mediated rapid metabolic and physiological responses of resistant and susceptible Sumatran fleabane [Conyza sumatrensis (Retz.) E. Walker; syn.: Erigeron sumatrensis Retz.] to 2,4-D herbicide. Fixed conditions (25 °C and 65 ±5% relative humidity), we assayed injury symptoms, chlorophyll a fluorescence and antioxidative systems of both resistant and susceptible biotypes to 2,4-D (1005 g a.e. ha-1). Under 15°C vs 25°C temperatures and light and dark conditions, oxidative stress-mediated damage was assayed on plants that received 2,4-D herbicide applications. The injury symptoms observed in the 2,4-D resistant biotype were rapid necrosis in leaves within 30 min, with the re-establishment of normal growth within 1- to 2-weeks after 2,4-D treatment. The basal antioxidant enzyme activities of superoxide dismutase (SOD), catalase (CAT), and ascorbate peroxidase (APX) in the resistant biotype were greater than to the susceptible, though the activities of all enzymes generally did not differ between untreated and treated in the resistant biotype. The resistant biotype showed great reduction (at 1 and 4 h after application) in the photosynthetic electron transport chain performance index, while in the susceptible biotype these metabolic changes were detected only after 4 h. The resistant biotype recovered from the foliar damage 1- to 2-weeks after 2,4-D application, while the susceptible biotype was controlled. The production of H2O2 was responsive to temperature and increased faster in the 2,4-D-resistant biotype than in the susceptible one at both 15°C and 25°C; however, there was a greater increase at 25°C in the resistant biotype. The H2O2 production was not light-dependent in 2,4-D-resistant C. sumatrensis, with increases even under dark conditions. The 2,4-D resistant biotype showed rapid photosynthetic damage, possibly due to the rapid necrosis and leaf disruption, and increased the H2O2 content compared to the susceptible biotype.

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.