Pinoxaden is a POST acetyl coenzyme A carboxylase (ACCase) inhibitor in the phenylpyrazolin chemical family and is labelled for turfgrass use at broadcast rates of 35.5 to 71 g ai ha−1 and spot spray rates of 156 to 310 g ai ha−1. A greenhouse rate-response study was conducted to characterize the efficacy of pinoxaden against common grassy weeds. Weed species examined in this study were yellow foxtail, southern sandbur, annual bluegrass, roughstalk bluegrass, large crabgrass, dallisgrass, bahiagrass, goosegrass, and perennial ryegrass. Nonlinear regressions were modelled to determine visible injury rates (the application rate at which 50% of the weed species were injured and the 90% [I90] rate) and weight reduction rates (the application rate at which there was a 50% reduction in fresh weight and 90% reduction [WR90]) for each weed species. Only annual bluegrass, bahiagrass, and goosegrass had visible injury I90 values greater than the maximum labelled spot spray rate of 310 g ai ha−1. Annual bluegrass, bahiagrass, southern sandbur, and goosegrass all had WR90 values greater than the maximum labelled spot spray rate of 310 g ai ha−1. Results from this study indicate that the evaluated weed species can be ranked, according to visible injury I90 values, from most to least susceptible: perennial ryegrass > yellow foxtail > dallisgrass > large crabgrass > southern sandbur > roughstalk bluegrass > bahiagrass > goosegrass > annual bluegrass.

Management of volunteer glyphosate-resistant (GR) corn may be problematic in soybean resistant to glyphosate and 2,4-D or dicamba, as auxinic herbicides often antagonize graminicide efficacy. Field and greenhouse trials were conducted using mixtures of 2,4-D or dicamba in combination with glyphosate and clethodim-A (formulated without an adjuvant) or clethodim-SM (adjuvant-inclusive formulation) to determine the effect on volunteer GR corn control. Neither auxinic herbicide reduced clethodim efficacy, regardless of clethodim rate or formulation in field trials. However, the addition of glyphosate to these mixtures at the 35 g ai ha−1 clethodim dose reduced control from clethodim-A and clethodim-SM by 62% to 75% and 27% to 47%, respectively. Increasing the clethodim dose to 105 g ha−1 or greater in combination with glyphosate and either auxinic herbicide generally restored clethodim efficacy (74% to 98% control); in one site-year, the addition of glyphosate plus dicamba to clethodim-A at 140 g ha−1 still reduced control by 34%. In greenhouse experiments, clethodim-A efficacy was reduced by 17% and 28% when applied with glyphosate plus 420 and 1,680 g ae ha−1 2,4-D, respectively, in the absence of crop oil concentrate (COC). Increasing the dose of dicamba in a similar mixture had a negligible effect. Irrespective of auxinic herbicide dose, the inclusion of COC to clethodim-A mixtures with glyphosate plus 2,4-D or dicamba resulted in ≥ 90% control. These results specify an enhanced risk of reduced clethodim efficacy on volunteer GR corn when glyphosate is added to mixtures containing 2,4-D or dicamba. To optimize control from these mixtures, clethodim should be applied at ≥ 105 g ha−1 and should include an activator adjuvant in the form of COC and/or an adjuvant-inclusive clethodim formulation. This recommendation contrasts with several labels of clethodim that do not require COC when applied with adjuvant-loaded glyphosate products.

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.

Field experiments were conducted in 2014 and 2015 in Fayetteville, Arkansas, to evaluate the residual activity of acetyl-CoA carboxylase (ACCase)–inhibiting herbicides for monocot crop injury and weed control. Conventional rice, quizalofop-resistant rice, grain sorghum, and corn crops were evaluated for tolerance to soil applications of six herbicides (quizalofop at 80 and 160 g ai ha–1, clethodim at 68 and 136 g ai ha–1, fenoxaprop at 122 g ai ha–1, cyhalofop at 313 g ai ha–1, fluazifop at 210 and 420 g ai ha–1, and sethoxydim at 140 and 280 g ai ha–1). Overhead sprinkler irrigation of 1.3 cm was applied immediately after treatment to half of the plots, and the crops planted into the treated plots at 0, 7, and 14 d after herbicide treatment. In 2014, injury from herbicide treatments increased with activation for all crops evaluated, except for quizalofop-resistant rice. At 14 d after treatment (DAT) in 2014, corn and grain sorghum were injured 19% and 20%, respectively, from the higher rate of sethoxydim with irrigation activation averaged over plant-back dates. Conventional rice was injured 13% by the higher rate of fluazifop in 2014. Quizalofop-resistant rice was injured no more than 4% by any of the graminicides evaluated in either year. In 2015, a rainfall event occurred within 24 h of initiating the experiment; thus, there were no differences between activation via irrigation or by rainfall. However, as in 2014, grain sorghum and corn were injured 16% and 13%, respectively, by the higher rate of sethoxydim, averaged over plant-back dates. All herbicides provided little residual control of grass weeds, mainly broadleaf signalgrass and barnyardgrass. These findings indicate the need to continue allowing a plant-back interval to rice following a graminicide application, unless quizalofop-resistant rice is to be planted. The plant-back interval will vary by graminicide and the amount of moisture received following the application.

Research was conducted to determine foliar absorption of 14C-clethodim and its polar degradation products with five adjuvants and to compare the relative herbicidal activity of clethodim and its polar degradation products. Differential 14C-clethodim and 14C-polar degradation products absorption occurred among the five adjuvants. Adjuvants that mediated rapid foliar absorption of clethodim did not always mediate rapid foliar uptake of polar degradation products. Herbicidal activity of clethodim exceeded activity of polar degradation products regardless of time of day of application or whether adjuvant was used. Inclusion of adjuvant was required for herbicidal activity of polar degradation products. Clethodim activity declined when applied at 0800 h EDT compared to applications at 2000 h EDT. To maximize herbicidal activity of clethodim, adjuvants should be selected that mediate rapid foliar absorption of both clethodim and the polar degradation products of clethodim and that minimize photodegradation of clethodim.

Field and growth chamber experiments were conducted to investigate the influence of emulsifiable mineral oil, emulsifiable rapeseed oil, and the emulsifier (polyoxyethylene C13/C15 oxo alcohol) on the efficacy of phenmedipham and metoxuron against common lambsquarters, and of sethoxydim and the ethyl ester of quizalofop against winter wheat. In field studies, mineral oil and rapeseed oil were equally effective in increasing the efficacy of phenmedipham (0.24 and 0.48 kg ai/ha), metoxuron (0.6 and 1.2 kg ai/ha), and sethoxydim (0.05 and 0.1 kg ai/ha), but mineral oil was superior to rapeseed oil with quizalofop. In growth chamber studies, mineral oil and rapeseed oil were equally effective in increasing the efficacy of metoxuron, sethoxydim, and quizalofop-ethyl, but rapeseed oil was more effective than mineral oil with phenmedipham. Both in the field and in the growth chamber, the emulsifier was at least as effective as the oil adjuvants, when combined with all herbicides except sethoxydim. The herbicide doses giving 50% response (ED50) were determined for the growth chamber experiments. The adjuvants reduced the ED50 2.7-fold with phenmedipham, 51-fold with metoxuron, 2.7-fold with sethoxydim, and 6.8-fold with quizalofop when averaged over the three adjuvants. It was concluded that rapeseed oil (all tested herbicides except quizalofop) or the emulsifier (all tested herbicides except sethoxydim) can serve as a substitute for mineral oil.

Greenhouse and field experiments were conducted from 1987 to 1990 at the Lacombe Research Station to determine the influence of ammonium sulfate (AS) on various grass control herbicides. In field studies, AS had slight or no effects on the phytotoxicity of aryloxyphenoxypropanoate (APP) herbicides (fenoxaprop, fluazifop, haloxyfop, and quizalofop). The largest AS-mediated increase in APP herbicide phytotoxicity was 19% (based on fresh weight reduction) for wild oat with haloxyfop at 50 g/ha. AS consistently mediated increases in cyclohexanedione (CHD) herbicide phytotoxicity. With added AS, barley fresh weight was reduced 75% (1988) with BAS 517 at 50 g/ha, and 100% (1990) with clethodim at 25 g/ha. Greenhouse studies confirmed field studies, but differences were less substantial and consistent. It is suggested that APP herbicides are either less susceptible to UV degradation than CHD herbicides, and/or that APP herbicides may penetrate plant cuticles quickly enough to nullify any protection from UV degradation that AS might provide via rapid absorption.

The herbicide pinoxaden is a phenylpyrazoline inhibitor of acetyl coenzyme A carboxylase. Research was conducted to determine the effects of pinoxaden (90 g ai ha−1) alone and in combination with herbicide safeners on creeping bentgrass injury as well as perennial ryegrass and roughstalk bluegrass control. Greenhouse experiments determined that herbicide safeners cloquintocet-mexyl, fenchlorazole-ethyl, and mefenpyr-diethyl were more effective in reducing creeping bentgrass injury from pinoxaden than benoxacor, isoxadifen-ethyl, and naphthalic-anhydride. Other experiments determined that creeping bentgrass injury from pinoxaden decreased as rates (0, 23, 45, 68, 90, 225, or 450 g ha−1) of cloquintocet-mexyl, fenchlorazole-ethyl, and mefenpyr-diethyl increased. On the basis of creeping bentgrass responses to various safener rates, safeners were applied at 68 and 450 g ha−1 in additional experiments to evaluate their effects on pinoxaden (90 g ha−1) injury to creeping bentgrass and efficacy against perennial ryegrass and roughstalk bluegrass. In these experiments, safeners mefenpyr-diethyl and cloquintocet-mexyl reduced pinoxaden-induced creeping bentgrass injury (from 25 to ≤ 5%) more than fenchlorazole-ethyl at 2 wk after treatment. Safeners reduced pinoxaden efficacy against roughstalk bluegrass. Perennial ryegrass was controlled > 80% by pinoxaden and herbicide safeners did not reduce control. Field experiments should evaluate pinoxaden in combination with cloquintocet-mexyl and mefenpyr-diethyl to optimize safener : herbicide ratios and rates for creeping bentgrass safety as well as perennial ryegrass and roughtstalk bluegrass control in different climates and seasons.

A Lolium multiflorum Lam. biotype resistant to diclofop-methyl was found in a Triticum aestivum field in France (Normandy) that had been treated for several years with diclofop-methyl. Based on plant survival evaluated 21 d after herbicide application, the biotype exhibited a high level of resistance to diclofop-methyl and moderate resistance to CGA-184927-propargil and PP-604. The resistant biotype exhibited a small increase in tolerance to haloxyfop-methyl, quizalofop-ethyl, sethoxydim, and BAS-517-H, but was controlled by recommended field rates for these herbicides. The mechanism of resistance was investigated for diclofop-methyl. There was little or no difference in diclofop-methyl absorption by leaves of resistant and susceptible biotypes measured 48 h after treatment. For both biotypes, less than 1% of absorbed radiolabel was translocated during 48 h following foliar application of 14C-diclofop-methyl. Metabolism of diclofop-methyl was not significantly altered in the resistant biotype. In both biotypes, diclofop-methyl was rapidly metabolized to diclofop acid followed by a slow rate of formation of a polar conjugate. Two multifunctional acetyl coenzyme A carboxylase isoforms (ACCase I and ACCase II) were isolated from leaf tissue of resistant and susceptible biotypes. Both isoforms exhibited a subunit molecular mass of 203 kDa. For both resistant and susceptible biotypes, ACCase I constituted approximately 80% of total ACCase activity. Graminicide concentrations required to inhibit ACCase activity by 50% (I50 values) were determined for both ACCase isoforms from resistant and susceptible biotypes. The ACCase II isoform was highly resistant to graminicides in both biotypes. In contrast, the I50 value for diclofop inhibition of ACCase I was 19-fold greater for the enzyme isolated from the resistant biotype compared with the susceptible biotype. It is concluded that diclofop resistance in the L. multiflorum biotype from Normandy is caused by the presence of a resistant form of the ACCase I isoform.

Bermudagrass and goosegrass are problematic weeds with limited herbicides available for POST control in creeping bentgrass. Metamifop effectively controls these weeds with greater selectivity in cool-season grasses than other ACCase inhibitors. The objectives of this research were to determine the physiological basis for metamifop selectivity in turfgrasses. In greenhouse experiments, metamifop rate required to reduce shoot biomass 50% from the nontreated (GR50) at 4 wk after treatment was > 6,400, 2,166, and 53 g ai ha−1 for creeping bentgrass, Kentucky bluegrass, and goosegrass, respectively. The GR50 for bermudagrass treated with diclofop-methyl or metamifop was 2,850 and 60 g ha−1, respectively. In laboratory experiments, peak absorption of 14C-metamifop was reached at 48, 72, and 96 h after treatment (HAT) for goosegrass, creeping bentgrass and Kentucky bluegrass, respectively. Grasses translocated < 10% of the absorbed radioactivity out of the treated leaf at 96 HAT, but creeping bentgrass translocated three times more radioactivity than goosegrass and Kentucky bluegrass. Creeping bentgrass, Kentucky bluegrass, and goosegrass metabolized 16, 14, and 25% of 14C-metamifop after 96 h, respectively. Goosegrass had around two times greater levels of a metabolite at retention factor 0.45 than creeping bentgrass and Kentucky bluegrass. The concentration of metamifop required to inhibit isolated ACCase enzymes 50% from the nontreated (I50) measured > 100, > 100, and 38 μM for creeping bentgrass, Kentucky bluegrass, and goosegrass, respectively. In other experiments, foliar absorption of 14C-metamifop in bermudagrass was similar to 14C-diclofop-methyl. Bermudagrass metabolized 23 and 60% of the absorbed 14C-diclofop-methyl to diclofop acid and a polar conjugate after 96 h, respectively, but only 14% of 14C-metamifop was metabolized. Isolated ACCase was equally susceptible to inhibition by diclofop acid and metamifop (I50 = 0.7 μM), suggesting degradation rate is associated with bermudagrass tolerance levels to these herbicides. Overall, the physiological basis for metamifop selectivity in turfgrass is differential levels of target site inhibition.

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.

Two studies consisting of six field experiments each were conducted at three locations in southwestern Ontario, Canada, in 2014 and 2015 to evaluate the possible antagonism when dicamba was added to quizalofop-p-ethyl or clethodim for the control of volunteer glyphosate-resistant (GR) corn. At 4 wk after application (WAA), quizalofop-p-ethyl at 24, 30, or 36 g ai ha−1 provided 88, 94, and 95% control of volunteer GR corn, respectively. The addition of dicamba at 300 or 600 g ae ha−1 to quizalofop-p-ethyl (24 g ha−1) reduced the activity of quizalofop-p-ethyl on volunteer GR corn by 12 and 20%. At 4 WAA, clethodim at 30, 37.5, and 45 g ai ha−1 provided 85, 91, and 95% control of volunteer GR corn, respectively. The addition of dicamba at 300 or 600 g ha−1 to clethodim (30 g ha−1) resulted in antagonism, causing a reduction in volunteer GR corn by 12 and 11%, respectively. In general, there was greater antagonism when the high rate of dicamba was tank-mixed with the lower rate of the graminicide. There was no antagonistic effect on soybean yield by tank-mixing dicamba with either graminicide at all rates evaluated. Based on these results, volunteer GR corn can be controlled effectively by increasing the rate of the graminicide when tankmixed with dicamba.

Field experiments were conducted in Auburn, AL in 2008 and 2009 to assess new aryloxyphenoxypropionate (AOPP) herbicides applied alone and tank-mixed with triclopyr for Tifway bermudagrass control in Zorro zoysiagrass. Treatments included three sequential applications of clodinafop (0.07 kg ai ha−1); triclopyr (1.12 kg ae ha−1); clodinafop + triclopyr (0.07 + 1.12 kg ha−1); fenoxaprop (0.10 kg ai ha−1); fenoxaprop + triclopyr (0.10 + 1.12 kg ha−1); metamifop (0.40 kg ai ha−1); and metamifop + triclopyr (0.40 + 1.12 kg ha−1). Clodinafop, fenoxaprop, and metamifop applied alone controlled Tifway bermudagrass 32 to 65% when rated 3 wk after the final application; however, the addition of triclopyr to these AOPP herbicides increased bermudagrass control to ≥ 89%. All AOPP herbicides applied alone caused unacceptable injury to Zorro zoysiagrass (20 to 42%) 3 wk after the final application. Clodinafop resulted in the greatest zoysiagrass injury (42%), whereas metamifop caused moderate injury (20%). Zorro zoysiagrass exhibited less injury (< 3%) and greater turf coverage (≥ 95%) when AOPP herbicides were tank-mixed with triclopyr. Of the three AOPP herbicides evaluated in this study, only fenoxaprop is currently labeled for use on turfgrass. However, the nonlabeled herbicides (clodinafop and metamifop) provided bermudagrass control and zoysiagrass safety equal to the commercial standard (fenoxaprop) 3 wk after the final application when tank-mixed with triclopyr. Where zoysiagrass is contaminated with bermudagrass, turf managers will likely have to make applications of AOPP herbicides tank-mixed with triclopyr over multiple years to control bermudagrass as it will continue to regrow from deep rhizomes.