Inheritance of resistance to diclofop was studied in three wild oat biotypes (designated B, C., and H) from the Willamette Valley of Oregon. Cultivated oat (cultivar ‘Monida’) was crossed, including reciprocals, to three wild oat biotypes. Leaves of each F1 plant were spotted with diclofop as a nondestructive test for resistance or susceptibility. All F1 hybrids were resistant, indicating that resistance is dominant and is under nuclear control. The F2 plants where Monida was the maternal parent were screened with diclofop, and F2 plants of the Monida/C cross were screened with fenoxaprop because the parent C biotype was resistant to fenoxaprop. At lower doses, a 3:1 (R:S) segregation ratio in F2 was observed and at higher doses a 1:3 (R:S) segregation ratio was often observed. The F2:3 families segregated in a 1:2:1 (all resistant : segregating resistant and susceptible all susceptible) ratio when treated with a 1.1-kg ae ha−1 dose of diclofop. This confirms that resistance to diclofop in the B, C, and H biotypes is primarily under monogenic control, with resistance being dominant to susceptibility at lower herbicide doses. At increased doses, susceptibility becomes dominant. Knowledge of the inheritance of resistance may help in the development of containment measures to prevent the spread of herbicide-resistance genes.

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.

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.

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.

Field research was conducted in 2010 and 2011 to investigate the efficacy of herbicides for dallisgrass control when applied at various growing (GDD) or cooling degree day (CDD) –based application timings. Herbicide treatments included fluazifop-p-butyl (fluazifop; 105 g ai ha−1), mesotrione (280 g ai ha−1), tembotrione (92 g ai ha−1), topramezone (37 g ai ha−1), and tank mixtures of fluazifop plus mesotrione, tembotrione, or topramezone. Herbicide treatments were applied at either 75, 175, 375, 775 GDD, or 5 CDD. Treated plots were subjected to three tall fescue interseeding regimes: no seeding, seeding in spring, or seeding in fall (0, 353, and 353 kg pure live seed ha−1, respectively). In 2010, dallisgrass control from fluazifop applied at 75, 375, and 775 GDD was poor (< 50%) by 52 wk after treatment (WAT); in 2011, control from fluazifop application at these timings was higher (62 to 72%). When applied at 175 GDD or 5 CDD in 2010 and 2011, dallisgrass control from fluazifop ranged from 79 to 93% at 52 WAT. The addition of mesotrione, tembotrione, or topramezone to fluazifop did not affect dallisgrass control at any application timing, and control provided by these herbicides alone was low (< 65%). Interseeding tall fescue in the fall improved dallisgrass control from herbicides applied at 75 GDD in 2010 and 175, 375, and 775 GDD at 52 WAT in both years. Results suggest that timing of fluazifop applications at 175 GDD and 5 CDD enhances dallisgrass control.

Metamifop is an aryloxyphenoxypropionate herbicide under evaluation in the United States for annual grass control in cool-season turfgrasses. Insufficient information is available on the most effective metamifop application timings and mixtures for POST smooth crabgrass control. Field trials conducted in Blacksburg, VA, evaluated metamifop for smooth crabgrass control in existing stands of perennial ryegrass, Kentucky bluegrass, and tall fescue at three rates compared to fenoxaprop, metamifop applied twice at three application intervals, and metamifop in combination with the broadleaf herbicides carfentrazone, 2,4-D plus dicamba plus mecoprop (DDM), and mesotrione. Smooth crabgrass control was equivalent with metamifop at 400 g ai ha−1 and fenoxaprop at 195 g ai ha−1. Smooth crabgrass cover was 2% or less, 12 wk after initial treatment, when treated twice with metamifop (300 g ha−1) at a 3-, 6-, or 8-wk interval and significantly better than metamifop applied once. Smooth crabgrass cover was significantly greater at every assessment date in plots treated with metamifop plus DDM than all other metamifop plus broadleaf herbicide admixtures. Metamifop did not appear to significantly injure any turfgrass in these studies, but conclusions about metamifop safety to cool-season turfgrasses cannot be made from these studies due to nonreplication of turfgrass species. According to these data, metamifop is an effective herbicide for controlling smooth crabgrass in cool-season turfgrasses when applied once at 300 or 400 g ha−1 or twice at a 3-, 6-, or 8-wk interval. Although metamifop continues to control smooth crabgrass when added to some broadleaf herbicides, smooth crabgrass control was reduced when metamifop was combined with DDM.

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.