Managing winter annual grass weeds has long been a challenge in the dryland regions of the Pacific Northwest (PNW) where soft white winter wheat is grown. The recent development of quizalofop-resistant (CoAXium) wheat varieties allows growers to use quizalofop (QP), a herbicide that inhibits acetyl-CoA carboxylase (ACCase) for postemergence grass control. Field experiments were conducted over two winter wheat growing seasons in 2021–2022 and 2022–2023 near Adams, OR, to evaluate QP efficacy on feral rye and for crop safety. Downy brome and jointed goatgrass control with QP were assessed in 2021–2022 and 2022–2023, respectively. QP treatments provided effective control of feral rye (≥95%), downy brome (≥87%), and jointed goatgrass (99%) regardless of rate, adjuvant, and spray volume tested. Spring-applied QP caused no injury to winter wheat. Results indicate that the QP-resistant wheat technology can help PNW wheat growers selectively control winter annual grasses.

Quizalofop-resistant rice allows for over-the-top applications of quizalofop, a herbicide that inhibits acetyl-coenzyme A carboxylase. However, previous reports have indicated that quizalofop applied postemergence may cause significant injury to quizalofop-resistant rice. Therefore, field experiments were conducted to evaluate the response of quizalofop-resistant rice cultivars to quizalofop applications across different planting dates. Under controlled conditions, the effects of soil moisture content, air temperature, and light intensity on quizalofop-resistant rice sensitivity to quizalofop were investigated. In the planting date experiment, injury of more than 11 percentage points was observed on early-planted rice compared with late-planted rice at the 5-leaf stage, with higher injury observed under saturated soil conditions. However, quizalofop applications at the labeled rate caused ≤16% reduction in yield regardless of planting environment. Quizalofop-resistant cultivars exhibited more injury by at least 25 percentage points when soil was maintained at 90% or 100% of field capacity because rice cultivars ‘PVL01’, ‘PVL02’, and ‘RTv7231 MA’ exhibited ≥42%, 30%, and ≥54% injury, respectively, compared with ≤10%, ≤5%, and ≤22% injury, respectively, at 40% or 50% of field capacity, pooled over rating timing. Greater injury ranging from 18% to 31% was observed on quizalofop-resistant rice grown under low light intensity (600 µmol m−2s−1) compared with 5% to 14% injury under high light intensity (1,150 µmol m−2s−1). The injury persisted from 7 to 28 d after 5-leaf stage application (DAFT), averaged over quizalofop-resistant cultivars and air temperatures (20/15 C and 30/25 C day/night, respectively). At 7 DAFT, greater injury (by 5 to 21 percentage points) was observed on quizalofop-resistant cultivars; PVL01, PVL02, and RTv7231 MA exhibited 33%, 9%, and 58% injury, respectively, under 20/15 C temperature conditions compared with 13%, 4%, and 37% injury, respectively, under 30/25 C day/night conditions averaged over light intensities. Overall, quizalofop is likely to cause a greater risk for injury to quizalofop-resistant rice if it is applied under cool, cloudy, and moist soil conditions.

Zoysia germplasm exhibit different levels of sensitivity to fluazifop-P-butyl, but the genetic factors responsible for such differences are unknown. Segregation patterns of the fluazifop-P-butyl tolerance trait were studied under greenhouse conditions. In total, 244 F1 lines were generated from multiple crosses between the tolerant line 5337-2 (non–target site tolerance) and three more-sensitive lines (123, 252, and 5330-23). Progeny segregation showed that fluazifop-P-butyl tolerance within zoysiagrass (Zoysia spp.) is expressed as a quantitative trait with a wide range of intermediate phenotypes between parental phenotypes. Transgressive segregation was extensive and largely favored susceptibility in most families, but was especially evident for 5337-2 × 123 and 5337-2 × 5330-23. The segregation patterns for biomass reduction and percent injury were different within reciprocal crosses and among three different family crosses. Reciprocal effects were observed in growth reduction for 5337-2 × 5330-23, in percent injury at 3 wk after the treatment (WAT), and for 5337-2 × 252 at 6 WAT. This indicated that fluazifop-P-butyl tolerance was not completely controlled by nuclear genetic factors in 5337-2 and maternal/cytoplasmic inheritance was also partially responsible. These results suggested that fluazifop-P-butyl tolerance may be attributed to multiple genetic mechanisms, which could present a challenge for future breeding efforts because of the difficulty of fixing multiple traits within a breeding population.

Breeding herbicide tolerance into new cultivars can improve safety and weed control in turfgrass systems. The sensitivity to fluazifop-P-butyl of 27 zoysiagrass (Zoysia spp.) lines was screened under greenhouse conditions to identify potential tolerant germplasm for breeding programs. The herbicide rate that caused 50% biomass reduction (GR50) and the rate that caused 50% injury (ID50) were calculated to select the three most-tolerant and the five most-susceptible lines for studying the physiological mechanisms responsible for fluazifop-P-butyl tolerance. The differences in GR50 and ID50 between susceptible and tolerant lines ranged from 4-fold to more than 10-fold. Cytochrome P450–mediated metabolism was not detected in fluazifop-P-butyl–tolerant lines. Sequencing of the ACCase gene confirmed that none of the seven previously reported mutations conferring resistance to acetyl-CoA carboxylase (ACCase)-inhibiting herbicides in other species were present in any of the tolerant or susceptible zoysiagrass lines studied. An Ala-2073-Thr substitution was identified in two tolerant lines, but this mutation did not completely explain the tolerant phenotype. No clear differences in absorption and translocation rates of 14C-radiolabeled fluazifop-P-butyl were observed among most lines, with the exception of a susceptible line that exhibited greater translocation than two of the tolerant lines. Metabolite profiles did not differ between tolerant and susceptible lines. Our results suggest that the diversity in tolerance to fluazifop-P-butyl in zoysiagrass germplasm is most likely the result of a combination of different, minor, additive non–target site mechanisms such as translocation rate and compartmentation after absorption.

Diclofop–methyl and haloxyfop–methyl (0.001 to 10 μM) caused 9 to 61% inhibition of 14C–acetate incorporation into lipids in corn leaf segments within 1 h of herbicide treatment, while neither herbicide affected this process in bean leaf segments. The herbicides did not affect 14C-malonate incorporation into lipids in corn leaf segments. Diclofop-methyl and haloxyfop-methyl reduced 14C-acetate incorporation into polar lipids and triglycerides in corn while incorporation into sterols was increased. In vitro activity of acetyl-coenzyme A carboxylase (EC 6.4.1.2) was inhibited from 26 to 94% within 5 min of exposure to the herbicides (1 to 10 μM). Diclofop acid inhibited this enzyme activity more than did haloxyfop acid. Differences in field activity between diclofop-methyl and haloxyfop-methyl are not related to differential sensitivity of acetyl–coenzyme A carboxylase to the two herbicides.

Antagonism of quizalofop-P efficacy on annual grasses by bromoxynil has been noted in both the field and greenhouse. Laboratory experiments were conducted on yellow foxtail (Setaria glauca) to determine the effect of mixing bromoxynil with the ethyl ester of quizalofop-P on absorption, translocation, and metabolism of 14C-quizalofop-P Applying bromoxynil in mixture with quizalofop-P reduced 14C-label absorption from 63 to 51%, 73 to 52%, 77 to 68%, and 90 to 80% at 4, 8, 24, and 96 h after treatment, respectively. Translocation of 14C-label from the treated leaf into the shoot above or shoot below was unaffected by bromoxynil. However, translocation into the roots was reduced from 0.9 to 0.4% and 1.0 to 0.5% at 4 and 8 h after treatment, respectively, but differences were not noted at 0.5, 1, 24, and 96 h after treatment. Bromoxynil increased deesterification of quizalofop-P-ethyl into quizalofop-P acid from 45 to 60% in the shoot above the treated leaf. However, bromoxynil did not affect metabolism of quizalofop-P in the treated leaf or shoot below the treated leaf. These results suggest that antagonism of quizalofop-P activity by bromoxynil is primarily due to decreased absorption of quizalofop-P, whereas effects on translocation and metabolism were minor.

In spring 2005, a downy brome population with possible resistance to fluazifop-P, an acetyl-CoA carboxylase (ACCase) inhibitor (group 1) herbicide was found in a commercial creeping red fescue seed production field, near La Grande, OR, where fluazifop-P had been used to control downy brome repeatedly over 7 yr. Greenhouse experiments were conducted to confirm resistance to a number of group 1 herbicides. The suspected resistant downy brome accession was tested for resistance to fluazifop-P and tested for cross-resistance to other aryloxyphenoxy propionate (APP) and cyclohexanedione (CHD) herbicides, including quizalofop-P, sethoxydim, and clethodim. Data recorded included plant-mortality counts and biomass. Tests revealed that the La Grande downy brome accession was highly resistant to fluazifop-P and sethoxydim at all tested rates. The La Grande accession suffered no mortality from fluazifop-P or sethoxydim treatments up to the maximum tested rate of eight times (8×) the labeled recommendation. The La Grande accession was resistant to quizalofop-P and clethodim at the labeled rate or less but was susceptible to application rates higher than the labeled rate. The control downy brome accession was completely susceptible to fluazifop-P, quizalofop-P, and clethodim at all rates and exhibited increasing susceptibility with increasing sethoxydim rate. This pattern of cross-resistance differs from that of a previously reported case of ACCase resistance in downy brome.

Greenhouse and laboratory experiments were conducted to determine the effect of CGA 362622 on the herbicidal activity of clethodim on goosegrass. CGA 362622 did not affect absorption and translocation of 14C-clethodim by goosegrass. Averaged across the two treatments of clethodim alone and clethodim plus CGA 362622, absorption was 27 and 85% of the applied 14C-clethodim at 0.5 and 96 h, respectively. By 96 HAT, only 0.8% of applied 14C had translocated to the shoot below the treated leaf. Metabolism of clethodim was not affected by the presence of CGA 362622. Three metabolites of clethodim were detected in treated tissue at all harvest intervals. By 96 HAT, 56% of absorbed 14C converted to a relatively polar form when clethodim was applied alone or in the presence of CGA 362622. One day after treatment, the photosynthetic rate in plants treated with CGA 362622 had decreased below the rate in the nontreated check and remained lower until 6 d after treatment. These data suggest that the antagonism of clethodim by CGA 362622 may result from CGA 362622 altering the photosynthetic rate of goosegrass and therefore the sensitivity of acetyl-coenzyme A carboxylase to clethodim.