Greenhouse trials were conducted to evaluate graminicidal resistance of selected ornamental grasses. Blue fescue cultivars ‘Blue Glow’, ‘Sea Urchin’, ‘Spring Blue’, and ‘Superba’ were resistant to 1× (medium use rate) and 2× rates of fenoxaprop, fluazifop-P, quizalofop, and sethoxydim, whereas fountain grass, ravenna grass, and switchgrass were sensitive. Minor (<20%) visible phytotoxicity was observed on some fescues treated with the 2× rate of fluazifop-P at 14 but not at 69 days after treatment (DAT). Fountain grass, ravenna grass, and switchgrass exhibited severe (>70%) phytotoxicity from all herbicides 69 DAT. Mortality of non-fescues ranged from 55% (fountain grass) to 96% (ravenna grass).

In greenhouse studies, the calculated I50 (herbicide application resulting in 50% inhibition of shoot regrowth) in tall fescue was approximately 0.004 kg/ha for both sethoxydim and haloxyfop. In red fescue, the I50 for sethoxydim and haloxyfop was 9.4 kg/ha and 0.04 kg/ha, respectively. As measured in crude cell extracts of tall fescue, incorporation of 14C-acetyl-coenzyme A into fatty acids was inhibited 62 and 71% by 10 μM sethoxydim and 10 μM haloxyfop, respectively. In red fescue, 10 μM haloxyfop inhibited 14C-acetyl-CoA incorporation into fatty acids by 29%, whereas 10 μM sethoxydim had no effect. The I50 for inhibition of acetyl-coenzyme A carboxylase activity in tall fescue with sethoxydim and haloxyfop was 6.9 and 5.8 μM, respectively. In red fescue the I50 for haloxyfop was 118 μM. Sethoxydim concentrations as high as 1 mM had little effect on acetyl-coenzyme A carboxylase activity in red fescue. These results suggest that acetyl-coenzyme A carboxylase is a sensitive site of action for sethoxydim and haloxyfop in tall fescue, and that tolerance to these herbicides in red fescue is due to the presence of a more tolerant form of the enzyme.

Resistance to fluazifop-P and quizalofop-P, (aryloxyphenoxypropionates) and sethoxydim (cyclohexanedione) was identified in 2 populations of johnsongrass in both field and greenhouse studies. The cropping history (1983–1991) of the sites indicated 1 or more annual applications of a graminicide (primarily fluazifop-P) since the early 1980s. Under field conditions, control of resistant seedling and rhizome johnsongrass (R91F) with fluazifop-P, quizalofop-P, fenoxaprop-ethyl, and sethoxydim was less than 35%. Clethodim provided up to 80% control of R91F. Under greenhouse conditions, ratios (R/S) of the I50 values (amount of herbicide required to inhibit plant growth by 50%) of resistant (2 sites: R91F and R91S) to susceptible (S91H) seedling (20–30-cm height) plants were > 388 (fluazifop-P), > 15 (quizalofop-P), and from 2.3 (R91S) to 3.4 (R91F) (both sethoxydim). For rhizome (30–45 cm height) plants, the R/S ratios were > 388 (fluazifop-P), > 16 (quizalofop-P), and 2.8 (R91S) to 8.5 (R91F) (both sethoxydim). Labeled rates (in kg ai ha−1) of fluazifop-P (0.10 and 0.21), quizalofop-P (0.039 and 0.08), and sethoxydim (0.21 and 0.21) were applied on seedling and rhizome plants, respectively, and resulted in little or no control of resistant johnsongrass. Greenhouse studies indicated registered rates of clethodim (0.10 and 0.14 kg ai ha−1 for seedling and rhizome plants, respectively) effectively controlled the resistant populations, but tolerance was measured for both seedling and rhizome plants at sublethal doses (down to 0.007 and 0.009 kg ai ha−1, respectively), with I50 ratios ranging from 1.5 (R91S) to 2.1 (R91F) for seedling plants and 4.5 (R91S) to 4.8 (R91F) for rhizome plants. Control of resistant seedling and rhizome johnsongrass under field conditions was adequate with glyphosate at 0.84, glufosinate at 0.84, and sulfosate at 0.84 kg ai ha−1, indicating no cross-resistance.

The purpose of this study was to determine cross-resistance patterns among wild oat lines resistant to acetyl-CoA carboxylase (ACCase) inhibitors and to determine which, if any, cross-resistant type was more common than another. Discriminatory concentrations of two aryloxyphenoxy-propionates (APP) and three cyclohexanediones (CHD) were determined using a petri-dish bioassay. These concentrations were then applied to 82 resistant wild oat lines identified in previous studies. In addition, two resistant standards (UM1 and UM33) and a susceptible standard (UM5) were included in the experiments. Coleoptile lengths expressed as percentages of untreated controls were used to assess the level of resistance to each herbicide. Large variations were observed among wild oat lines and herbicides. However, cluster analysis summarized the relationship between the five herbicides (variables) and the wild oat lines into three main cross-resistance types. Type A included wild oat lines with high resistance to APP herbicides and no or low resistance to CHD herbicides. Types B and C included those with low to moderate resistant and high levels of resistance to all five herbicides, respectively. Type C was the most common cross-resistance type. Relationships among herbicides were determined using pairwise correlation and principal component analysis (PCA). All correlations were high between APP herbicides and between CHD herbicides but not between APP and CHD herbicides. The first two axes of the PCA accounted for 88.4% of the total variance, with the first axis correlated to the CHD herbicides and the second axis correlated to the APP herbicides. In the PCA, wild oat lines were segregated into the three types identified in the cluster analysis. Although CHD and APP herbicides bind at the same region on the ACCase, resistant wild oat lines respond differently to them.

The objectives of this study were to determine the inheritance of aryloxyphenoxypropionate (APP) resistance in the wild oat population UM33 and to determine the genetic relationship between resistance in UM33 and another population, UM1, which has a different cross-resistance pattern. Reciprocal crosses were made between UM33 and a susceptible population UM5, and between UM33 and UM1. Initial screenings of F1 and F2 Is populations derived from crosses between UM33 and UM5 were conducted over a range of fenoxaprop-P rates to determine a discriminatory dosage. F2 populations and F2-derived F3 families were then screened at this dosage (1200 g ai ha−1) to determine segregation patterns. Results from reciprocal UM33 x UM5 F1 dose-response experiments, and F2 and F2-derived F3 segregation experiments indicated that UM33 resistance to fenoxaprop-P was governed by a single, partially dominant nuclear gene system. To determine if resistance in UM1 and UM33 results from alterations at the same gene locus, 584 F2 plants derived from reciprocal UM33 x UM1 crosses were screened with 150 g ha−1 fenoxaprop-P. This dosage was sufficient to kill susceptible plants (UM5), but was not sufficient to kill plants with a resistance allele from either parent. None of the treated F2 plants exhibited injury or death, indicating that UM1 and UM33 resistance genes did not segregate independently. From this it was concluded that resistance in both populations is encoded at the same gene locus.

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.

Resistance to the methyl ester of diclofop, an aryloxyphenoxypropionate graminicide, was shown for a wild oat (Avena fatua) population from Western Australia, and marked resistance to a range of aryloxyphenoxypropionate and cyclohexanedione graminicides was detected in a winter wild oat (Avena sterilis ssp. ludoviciana) population from South Australia. The A. sterilis biotype exhibited high levels of resistance to the aryloxyphenoxypropionate herbicides diclofop, fluazifop, haloxyfop, fenoxaprop, quizalofop, propaquizafop, and quinfurop and low levels of resistance to the cyclohexanedione herbicides sethoxydim, tralkoxydim, and cycloxydim. Ratios of LD50 values for responses of resistant and susceptible A. sterilis to the aryloxyphenoxypropionate herbicides were between 20 for propaquizafop and > 1,000 for fluazifop, and were between 2.5 and 3 for the cyclohexanedione herbicides. The LD50 value for diclofop for the A. fatua biotype was 442 g ai ha-1 which was 2.7-fold that of a susceptible control. Thirty-three percent of the plants survived at the registered rate of application.

Homozygous, sethoxydim-tolerant corn was field tested at two locations in 1989 and 1990. Sethoxydim at 0.22, 0.44, and 0.88 kg ha−1 was applied to sethoxydimtolerant corn in the 3- and 7-leaf stages. None of the sethoxydim treatments caused visible injury to the sethoxydim-tolerant corn, but all treatments were lethal to a parental corn line used as a control. Sethoxydim applied at either stage of corn development had no effect on number of days to 50% silk emergence, plant height, or grain yield, compared to nontreated plants. Sethoxydim-tolerant corn was also tolerant to mixtures of sethoxydim plus other postemergence herbicides that control dicotyledonous weeds. Sethoxydim mixed with atrazine or sethoxydim applied in sequential applications with dicamba or 2,4-D gave annual grass control similar to sethoxydim applied alone. However, the sethoxydim plus bentazon treatment resulted in reduced grass control in comparison to sethoxydim alone. When the broadleaf herbicides were mixed with sethoxydim or applied as sequential treatments, broadleaf weed control was the same as when the broadleaf herbicides were applied alone. The high level of corn tolerance to sethoxydim and the broad spectrum of weed control resulting from combinations of sethoxydim plus other postemergence herbicides indicates that sethoxydim-tolerant corn hybrids could increase the options available for weed control in corn.

A seed bioassay was developed and tested for the rapid identification of aryloxyphenoxypropionate (APP) and cyclohexanedione (CHD) resistance in wild oat. Two susceptible (S) genotypes, UM5 and Dumont, were treated with fenoxaprop-P and sethoxydim over a range of dosages on filter paper and agar. The former is a wild oat line and the latter a tame oat cultivar. Within 5 d, shoot and root development of both genotypes were completely inhibited by 10 μM fenoxaprop-P and 5 μM sethoxydim. These dosages were then tested to determine if they were suitable for distinguishing between resistant (R) and susceptible (S) plants. Agar medium was preferred over filter paper because of the ease of preparation and maintenance. Four known R wild oat populations were included in the tests. Those with high levels of resistance produced significantly longer coleoptiles and roots than S genotypes, but those with moderate or low levels of resistance could not be separated statistically from S biotypes based on quantitative measurements. However, after exposing the germinating, treated seeds to light for 24 to 48 h, all the R populations produced green coleoptiles and initiated a first leaf, unlike the S genotypes which did not turn green or produce any new growth. This procedure proved useful in discriminating between R and S genotypes and in ranking populations in terms of relative levels of resistance.

The first occurrences of wild oat resistance to diclofop in the Willamette Valley of Oregon were reported in 1990. Among eight resistant biotypes, GR50 values for diclofop were 3 to 64 times greater than the GR50 for a susceptible wild oat biotype. GR50 values for other aryloxyphenoxypropionate herbicides varied from 1 to over 100 times greater than a susceptible biotype. Only one resistant biotype was resistant to cyclohexanedione herbicides, and this was only a three-fold increase in GR50. Except for one biotype that had a low level of resistance to pronamide, none of the wild oat biotypes were cross-resistant to any other commonly used wild oat herbicide. Levels of resistance and cross-resistance did not follow a consistent pattern among biotypes in this study, suggesting more than one resistance trait. There were significant differences in the light use efficiency, height, dry weight, leaf area, and extent and timing of tillering and flowering of four wild oat biotypes studied. These physiological and morphological differences suggest that these resistant biotypes were selected independently. The diversity of resistance patterns and the coevolution of resistance at several locations will add to the difficulty of resistance management

The aryloxyphenoxypropionate and cyclohexanedione herbicides, which inhibit acetyl-coenzyme A carboxylase (EC 6.4.1.2), have also been hypothesized to act at specific sites on the plasmalemma. An impermeant sulfhydryl binding agent was reported to block the diclofop acid-induced depolarization of the membrane potential (Em) in rigid ryegrass. A correlation between the antagonistic interaction with auxin herbicides both in the field and in the Em response, and the repolarization of Em in herbicide-resistant rigid ryegrass following removal of diclofop acid also provide support for this hypothesis. However, similar membrane responses in resistant grasses and broadleaf species suggest that the membrane response may not be important in the phytotoxic activity of the postemergence graminicides under field conditions. In addition, an antagonistic interaction was not observed in roots of susceptible grasses exposed to combinations of diclofop-methyl and 2,4-D. Furthermore, the repolarization of the Em in diclofop-resistant rigid ryegrass was correlated to differential acidification of the external solution and an increase in the protonated form of diclofop acid, rather than a site-specific interaction at the plasmalemma. Although the membrane response is probably not involved in herbicide phytotoxicity in agricultural systems, a higher extracellular pH in the resistant biotypes of rigid ryegrass may inhibit the movement of these weak-acid herbicides across the plasmalemma, and possibly contribute to increased herbicide tolerance.

Resistance to fenoxaprop-P and other aryloxyphenoxypropionate and cyclohexanedione herbicides in the wild oat population, UM1, is controlled by a single, partially dominant, nuclear gene. In arriving at this conclusion, parents, F1 hybrids, and F2 plants derived from reciprocal crosses between UM1 and a susceptible wild oat line, UM5, were treated with fenoxaprop-P over a wide range of dosages. Based on these experiments, a dosage of 400 g ai ha−1 fenoxaprop-P was selected to discriminate between three response types. At this dosage, susceptible plants were killed and resistant plants were unaffected, whereas plants characterized as intermediate in response were injured but recovered. Treated F2 plants segregated in a 1:2:1 (R, I, S) ratio, indicative of single nuclear gene inheritance. This was confirmed by selfing F2 plants and screening several F3 families. Families derived from intermediate F2 plants segregated for the three characteristic response types, whereas those derived from resistant F2 plants were uniformly resistant. Chisquare analysis indicated the F2 segregation ratios fit those expected for a single partially dominant nuclear gene system. In addition, F2 populations from both crosses were screened with a mixture of fenoxaprop-Pand sethoxydim. The dosages of both herbicides (150 g ai ha−1 fenoxaprop-P and 100 g ha−1 sethoxydim) were sufficient to control only susceptible plants. Treated F2 populations segregated in a 3:1 (R:S) pattern, thereby confirming that resistance to the two chemically unrelated herbicides results from the same gene alteration.

Five classes of herbicides (carbamothioates, chloroacetamides, substituted pyridazinones, cyclohexanediones, and aryloxyphenoxypropionic acids) have been reported to inhibit lipid biosynthesis in higher plants. Carbamothioates impair the synthesis of surface lipids (waxes, cutin, suberin). These effects have been attributed to the ability of this herbicide class to inhibit one or more acyl-CoA elongases. Though as yet poorly characterized, these enzymes are associated with the endoplasmic reticulum and catalyze the condensation of malonyl-CoA with fatty acid acyl-CoA substrates to form very long-chain fatty acids used in the synthesis of surface lipids. There is contradictory evidence regarding the effects of chloroacetamide herbicides on de novo fatty acid biosynthesis. Selected substituted pyridazinones decrease the degree of unsaturation of plastidic galactolipids. This effect is attributed to the ability of selected members of this herbicide class to inhibit fatty acid desaturases which are thought to be located in the chloroplast envelope. Aryloxyphenoxypropionic acid and cyclohexanedione herbicides inhibit de novo fatty acid biosynthesis in grasses. The target site for these herbicide classes is the enzyme acetyl-CoA carboxylase which is found in the stroma of plastids. In most cases, selectivity between grasses and dicots is expressed at this site. Aryloxyphenoxypropionic acids and cyclohexanediones are reversible, linear, noncompetitive inhibitors of acetyl-CoA carboxylase from grasses. Both classes are also mutually exclusive inhibitors of grass acetyl-CoA carboxylase which suggests that they bind at a common domain on the enzyme.

Greenhouse and laboratory research was conducted to determine the antagonistic effects of various tank mixtures on BAS 625 efficacy. Bensulfuron at 60 g ai ha−1 and BAS 635 at 40 g ai ha−1 did not antagonize control of Echinochloa crus-galli or Brachiaria platyphylla by BAS 625 at 30 g ai ha−1 in greenhouse experiments. Tank mixtures of BAS 625 with 1,000 g ai ha−1 bentazon reduced BAS 625 control of E. crus-galli from 100 to 40%. Antagonism of BAS 625 activity by bentazon or chlorimuron at 10 g ai ha−1 was similar with B. platyphylla, reducing control from 100 to 28 and 32%, respectively. Addition of 5% (v/v) ethanol eliminated all antagonism with any of the herbicides used with either weed species. Uptake and translocation of 14C-BAS 625 1 and 12 h after treatment was not enhanced, either alone or in tank mixtures, with the addition of ethanol. Uptake of 14C-BAS 625 1 and 12 h after treatment was lower in both species when tank-mixed with bentazon. There was no effect of any of the antagonizing herbicides or ethanol on the metabolic degradation of the BAS 625 that was taken up by the plant. The herbicide concentration for 50% inhibition of activity (I50) for BAS 625 on Triticum aestivum acetyl coenzyme A carboxylase (ACCase) was 125 µM. Bentazon, BAS 635, and NC-311 at 1 mM each did not alter the inhibition on ACCase by BAS 625. BAS 635, NC-311, and bentazon at 1 mM inhibited the activity of ACCase 12, 16, and 29%, respectively. Our results indicate that antagonism of the weed control activity of BAS 625 by bentazon may be partly caused by reduced uptake. Other mechanisms may be involved to explain the antagonism of BAS 625 by bentazon and the sulfonylurea herbicides used in this study.

Herbicides targeting grass plastidic acetyl coenzyme A carboxylase (ACC) are effective selective graminicides. Their intensive use worldwide has selected for resistance genes in a number of grass weed species. Biochemistry and molecular biology have been the means of determining the herbicidal activity and selectivity toward crop plants of ACC-inhibiting herbicides. In recent years, elucidation of the tridimensional structure of ACC and identification of five amino acid residues within the ACC carboxyl transferase domain that are critical determinants for herbicide sensitivity shed light on the basis of ACC-based resistance to herbicides. However, metabolism-based resistance to ACC-inhibiting herbicides is much less well known, although this type of resistance seems to be widespread. A number of genes thus endow resistance to ACC-inhibiting herbicides, with the possibility for various resistance genes that confer dominant resistance at the herbicide field rate to accumulate within a single weed population or plant. This, together with a poor knowledge of the genetic parameters driving resistance, renders the evolution of resistance to ACC-inhibiting herbicides unpredictable. Future research should consider developing tactics to slow the spread of resistance. For this purpose, it is crucial that our understanding of metabolism-based resistance improves rapidly because this mechanism is complex and can confer resistance to herbicides with different target sites.

Acetyl-coenzyme A carboxylase (ACCase)–resistant Italian ryegrass is one of the most difficult-to-control weeds in United States wheat-production systems. Seed was collected from a suspected ACCase-resistant Italian ryegrass population in a winter wheat field with a history of ACCase-inhibitor herbicide use. This study investigated cross-resistance patterns in this Italian ryegrass population. Resistance was identified to the commercial dose of the ACCase herbicides pinoxaden, clethodim, sethoxydim, and clodinafop. Partial chloroplastic ACCase sequences revealed aspartate-to-glycine or isoleucine-to-asparagine substitutions at positions 2078 or 2041 in individuals of the resistant population. This is the first report, to our knowledge, of Asp-2078-Gly and Ile-2041-Asn substitutions in ACCase-resistant Italian ryegrass in the United States. Associating the occurrence of resistance alleles with resistance to specific active ingredients provides a better understanding of ACCase cross-resistance in Italian ryegrass and possibly options for its control.

A survey conducted across agricultural ecoregions of Saskatchewan in 1996 revealed that wild oat (Avena fatua) populations resistant to acetyl-CoA carboxylase (ACCase) inhibitors were present in approximately 10% of Saskatchewan fields (2.4 million ha). In the Aspen Parkland and Boreal Transition ecoregions, this increased to 17%. The objective of this study was to determine if agronomic practices promoted or delayed resistance and to assess producer awareness of herbicide resistance. Weed resistance and management questionnaire data from the 1996 resistance survey and management questionnaire data from the 1995 Saskatchewan weed survey were submitted to multiway frequency analysis. The frequency of occurrence of herbicide-resistant wild oat was related directly to ACCase inhibitor use. Resistance to cyclohexanedione (CHD) herbicides was not related to CHD use but to frequency of ACCase inhibitor use (i.e., CHD + aryloxyphenoxypropanoate [AOPP]), suggesting that the pressure imposed by AOPPs contributed to the selection of CHD resistance in wild oat. ACCase inhibitor use was more extensive in the Aspen Parkland and Boreal Transition ecoregions than in the Mixed and Moist Mixed Grassland ecoregions. Crop rotations were not conducive to rotation of herbicides with different sites of action. Frequency of ACCase inhibitor use increased with frequency of annual crops, in spite of the inclusion of cereal and dicot crops in the rotation. Producers utilizing conservation tillage practices in the Grassland ecoregions used proportionally more ACCase inhibitors than those using conventional tillage practices. This increase in ACCase use in conservation tillage systems did not result in an increased incidence of wild oat populations resistant to ACCase inhibitors. Producers reporting troublesome wild oat populations tended to have proportionally more ACCase-resistant wild oat. Producers who reported practicing weed sanitation were less likely to have resistant wild oat than those who were less careful. Increased awareness and implementation of management practices that will reduce the dependency on ACCase herbicides are required to better enable producers to prevent, delay, or manage herbicide-resistant wild oat populations.

During routine use of fluazifop-P-butyl for grass control, county extension agents in Georgia observed control of bristly starbur in grower fields. Experiments to characterize the activity of fluazifop-P-butyl on bristly starbur were conducted under greenhouse conditions in Gainesville, FL, during 2001 and 2002. Fluazifop-P-butyl activity was characterized as a function of herbicide rate and time after application. Commercially available fluazifop-P-butyl was compared to technical fluazifop-P-butyl as a function of herbicide rate and bristly starbur height. Finally, injury to bristly starbur was evaluated when clethodim, diclofop, fluazifop-P-butyl, haloxyfop, quizalofop-p, and sethoxydim were applied at two growth stages. Fluazifop-P-butyl caused >90% injury to bristly starbur with all other post graminicides displaying <8% injury. Nonlinear regression revealed a sigmoidal response of bristly starbur injury to fluazifop-P-butyl. Estimates for 50 and 90% bristly starbur injury (I50 and I90) were 0.07 and 0.14 kg ai/ha, respectively. There was no difference in activity of technical and commercial fluazifop-P-butyl formulations. There was a differential response of bristly starbur to fluazifop-P-butyl over time as a function of plant height at the time of treatment. However, 14 days after treatment (DAT) all treatments displayed >89% injury. Bristly starbur response to fluazifop-P-butyl was similar to injury associated with contact-type herbicides.

A biotype of green foxtail found in Spain exhibited cross-resistance among acetyl-CoA carboxylase (ACCase)–inhibiting herbicides. Field doses that totally inhibited shoot fresh weight in the susceptible (S) biotype were determined for six aryloxyphenoxypropionates (clodinafop, diclofop, fenoxaprop-P, fluazifop-P, haloxyfop-P, and propaquizafop) and six cyclohexanediones (clefoxydim, clethodim, cycloxydim, sethoxydim, tepraloxydim, and tralkoxydim). The resistant (R) biotype showed cross-resistance to all herbicides except fenoxaprop-P, propaquizafop, clefoxydim, and tepraloxydim. There were no differences in the absorption, translocation, and metabolism of [14C]diclofop between the S and R biotypes. On the basis of herbicide dose that inhibited ACCase activity by 50% (I50 values), ACCase of the R biotype was 5.8-, 13.9-, 20.0-, 102.4-, 416.7-, and 625.0-fold less sensitive to clethodim, haloxyfop, diclofop, fluazifop, cycloxydim, and sethoxydim, respectively, than that of the S biotype. Two multifunctional ACCase isoforms (ACCase I and ACCase II) were purified partially and separated. ACCase II was highly resistant to diclofop acid in both biotypes, with I50 values ranging between 92 and 95 μM. However, the I50 values observed for ACCase I revealed that the R biotype was 30.8-fold less sensitive to diclofop than the S biotype. These results suggest the mechanism of resistance in green foxtail to diclofop relates to an altered ACCase I isoform.

Volunteer Enlist corn with the AAD-1 (aryloxyalkanoate dioxygenase-1) transgene can become a problem when glyphosate-resistant (GR) soybean follows Enlist corn in the rotation. Field trials were conducted at Ridgetown, Ontario in 2013 and 2014 to evaluate the control of volunteer Enlist corn in GR soybean. Glyphosate plus clethodim at 30 g ai ha−1 provided 75 to 92% control of volunteer Enlist corn at 1, 2, 4, and 8 weeks after treatment application (WAT) and reduced volunteer Enlist corn density and dry weight 95 to 97%. Glyphosate plus clethodim at 60 g ai ha−1 provided 84 to 98% control of volunteer Enlist corn at 1, 2, 4, and 8 WAT and reduced volunteer Enlist corn density and dry weight 97 to 99%. Glyphosate plus sethoxydim at 150 g ai ha−1 provided 66 to 86% control of volunteer Enlist corn at 1, 2, 4, and 8 WAT and reduced volunteer Enlist corn density and dry weight 91 to 97%. Glyphosate plus sethoxydim at 300 g ha−1 provided 84 to 96% control of volunteer Enlist corn at 1, 2, 4, and 8 WAT and reduced volunteer Enlist corn density and dry weight 96 to 98%. Glyphosate plus fenoxaprop-p-ethyl, fluazifop-p-butyl, and quizalofop-p-ethyl applied POST provided 0 to 9% control of volunteer Enlist corn at 1, 2, 4, and 8 WAT and reduced volunteer Enlist corn density and dry weight 18 to 44%. Soybean yields closely reflected the level of volunteer Enlist corn control. Based on these results, the cyclohexanedione herbicides, clethodim and sethoxydim, provide adequate control of volunteer Enlist corn in GR soybean. In contrast, the aryloxyphenoxypropionate herbicides, fenoxaprop-p-ethyl, fluazifop-p-butyl and quizalofop-p-ethyl do not provide control of volunteer Enlist corn in GR soybean.