Gowan Company recently registered benzobicyclon, a WSSA Group 27 herbicide, as a postflood option in rice. It is the first 4-hydroxyphenylpyruvate dioxygenase-inhibiting herbicide commercially available in mid-southern U.S. rice production. In 2018 and 2019, field experiments were conducted across multiple sites in Arkansas to determine if the addition of benzobicyclon to quizalofop- or imidazolinone-resistant rice herbicide programs would improve weedy rice control. Across site-years, one application of quizalofop, either at the 1- or 3-leaf rice stage, followed by benzobicyclon applied postflood, provided comparable weedy rice control to two sequential applications of quizalofop, which is a standard herbicide program in quizalofop-resistant rice. Additionally, treatments containing quizalofop or quizalofop followed by benzobicyclon injured rice ≤5% at 28 d after the postflood application. Across site-years, at 28 d after the postflood application of benzobicyclon, all treatments containing a full-season herbicide program followed by benzobicyclon postflood provided comparable or improved weedy rice control when compared to two sequential early postemergence applications of imazethapyr. In both experiments, rice treated with benzobicyclon yielded comparably or better than treatments containing the standard herbicide program for each system. Findings from this research suggest that the use of benzobicyclon in quizalofop- and imidazolinone-resistant rice systems could be an additional and viable weedy rice control option for rice producers.

Weedy rice (WR) (Oryza spp.) is the most troublesome weed infesting rice paddies in Brazil. Several changes have occurred in this region regarding crop management, especially WR control based on the Clearfield® (CL) rice production system launched in 2003. This survey’s objective was to evaluate the WR infestation status by assessing the producers’ perception and the management practices used in southern Brazil after 18 yr of CL use in Brazil. Rice consultants and extension agents distributed a questionnaire to 213 producers in the Rio Grande do Sul (RS) and Santa Catarina (SC) states in the 2018 to 2019 growing season. In RS, most farms are larger than 150 ha, and farmers have adopted the CL system for more than 2 yr and use minimal or conventional tillage, permanent flooding, clomazone PRE tank-mixed with glyphosate at the rice spiking stage, and crop rotation with soybean [Glycine max (L.) Merr.] or pasture. In SC, rice farms are small, averaging from 20 to 30 ha, farmers predominantly plant pre-germinated rice and do not rotate rice with other crops, and roguing is practiced. Comparing both states, the CL system is used in 99.5% and 69.3% of the total surveyed rice areas in RS and SC, respectively. Imidazolinone-resistant WR is present in 68.4% and 26.6% of rice farms in RS and SC, respectively. Rice cultivation in Brazil is currently coexisting with WR with minimal integration of control methods. However, integrated practices can control this weed and are fundamental to the sustainability of systems based on herbicide-resistant rice cultivars.

Identification of common weeds is fundamental in determining adequate recommendations for management practices. The aim of this study was to identify the patterns of weed management adopted by rice farmers and the perspectives of consultants who work in flooded rice areas in Rio Grande do Sul (RS) State, Brazil. Fifty-three public and 50 private consultants who worked with rice in RS in 2017 and 2018 were interviewed. Data were analyzed by descriptive statistics. Both weedy rice and Echinochloa sp. occurred and escaped more often from chemical control because they remained in the field until harvest in 59% of the area. According to consultants, the main reasons for reduced weed control were related to herbicide resistance and late herbicide application. Fifty-six percent of farmers used imidazolinone herbicides at rates that were greater than those indicated on the label for POST application. The consultants’ main challenges were weed escapes, resistance management, and guidelines on herbicide rates. Survey results show that the use of herbicide rates above label recommendations and consultants’ work on control of weed escapes are directly related to the high occurrence of herbicide resistance.

Cereal rye (Secale cereale L.) control in wheat (Triticum aestivum L.) can be difficult with existing selective herbicides. High phenotypic diversity within populations coupled with suboptimal herbicide application conditions leads to varying degrees of control with herbicide treatments. The following research focused on the consequence of low temperature on imazamox fate in S. cereale. A greenhouse study was conducted to determine the number of warm-temperature days required for imazamox to control S. cereale. Absorption, translocation, and metabolism of imazamox was evaluated under warm (22/18C) and cold (4/4C) temperatures to identify changes to the fate of imazamox under different environmental conditions. In greenhouse conditions, more than 5 d of warm temperature following herbicide application was required to achieve 80% S. cereale mortality. Absorption of imazamox was reduced 20% when S. cereale was subjected to cold compared with warm temperatures. Only 10% of applied imazamox was moved from the treated leaf in continuous cool temperatures compared with greater than 60% in warm conditions. In cold conditions, imazamox content increased in all tested plant parts evaluated for the duration of the study, whereas in warm conditions, imazamox concentrations decreased in root and crown tissues after 3 d. Imazamox behavior was affected more by temperature than S. cereale growth stage. Secale cereale metabolism of imazamox was reduced, but not stopped in cold temperatures. After 6 d, only a 10% difference in intact imazamox remained between temperature treatments. In cold temperatures, reduced absorption and translocation, coupled with continued metabolism, allow plants to recover from an otherwise lethal imazamox treatment.

Effects of 0.1 M ammonium sulfate, 0.1 M potassium phosphate, and 7 g/ha of the isopropylamine salt of imazapyr {(+)-2-[4,5-dihydro-4-methyl-4-(1-methylethyl)-5-oxo-1H-imidazol-2-yl]-3-pyridinecarboxylic acid} were evaluated on the phytotoxicity of the ammonium salt of imazaquin {2-[4,5-dihydro-4-methyl-4-(1-methylethyl)-5-oxo-1H-imidazol-2-yl]-3-quinolinecarboxylic acid} and the ammonium salt of imazethapyr {(+)-2-[4,5-dihydro-4-methyl-4-(1-methylethyl)-5-oxo-1H-imidazol-2-yl]-5-ethyl-3-pyridinecarboxylic acid} applied postemergence to pitted morningglory (Ipomoea lacunosa L. #3 IPOLA). While each of these salts and imazapyr applied alone had no effect, combining them with imazaquin or imazethapyr significantly increased control of pitted morningglory.

Kochia growing on an industrial site where chlorsulfuron was applied repeatedly over several seasons was confirmed to be resistant to chlorsulfuron and several other acetolactate synthase (ALS) -inhibiting herbicides. In growth room experiments, resistant (R) plants were 2 to >180 times more resistant to five sulfonylurea herbicides and one imidazolinone herbicide (imazethapyr) than susceptible (S) plants, as measured by the ratio of dosages required to inhibit shoot dry matter accumulation by 50% (GR50 R/S). Similarly, in vitro assays of ALS activity indicated that from 3 to 30 times more herbicide was required to inhibit the enzyme from R plants than from S plants. Results of ALS enzyme assays indicated that R kochia was approximately equally resistant to metsulfuron, triasulfuron, and thifensulfuron, and 2.5 times more resistant to tribenuron than thifensulfuron. However, the response of R kochia growing in a spring wheat crop in the field was not consistent with results of the ALS enzyme assays. In field experiments, thifensulfuron at 32 g ai ha−1 had little effect on R kochia. In contrast, metsulfuron, triasulfuron, and tribenuron at 8 g ha−1 did not reduce R kochia seedling densities, but caused severe stunting such that 2 mo after treatment the shoot biomass of plants in untreated plots was four times greater than in sprayed plots. Herbicides with alternative modes of action including fluroxypyr, bromoxynil/MCPA ester, dichlorprop/2,4-D ester, and 2,4-D ester provided good control of R kochia in the field. Quinclorac did not reduce kochia densities, but surviving plants were stunted. To delay or avoid development of ALS inhibitor-resistant kochia populations, these alternative herbicides applied alone or in tank mixtures could be incorporated into a herbicide rotation.

Imazaquin and imazethapyr were applied postemergence to soybeans for control of 8- to 12-leaf rhizome johnsongrass and pitted morningglory in the field. At 8 weeks, johnsongrass control was 70% with 70 g ai/ha imazaquin plus 105 g ai/ha imazethapyr but was no more than 50% with a single application of either herbicide. Imazaquin at 70 g/ha plus imazethapyr at 35 g/ha interacted synergistically to provide 90% pitted morningglory control, while 140 g/ha imazaquin controlled 77%. Imazaquin at 70 g/ha with imazethapyr from 18 to 105 g/ha controlled both weed species equal to or better than that obtained with 140 g/ha imazaquin.

A false cleavers population that survived treatment with triasulfuron/bromoxynil in 1996 was identified in central Alberta, Canada, in a field that had been treated with acetolactate synthase (ALS) inhibitors in 3 of the previous 6 yr. In greenhouse studies, this biotype was highly resistant to the ALS inhibitors triasulfuron, thifensulfuron/tribenuron, and sulfometuron and moderately resistant to imazethapyr; GR50, values were > 16, > 5, > 1.0, and 9.9, respectively. In addition, cross-resistance was identified to the auxin-type herbicide quinclorac (GR50 value > 6.7) but not to fluroxypyr (GR50 value 1) or MCPA/mecoprop/dicamba. Quinclorac had not been used previously in this field. Analysis of ALS extracted from the resistant biotype and a susceptible biotype from a nearby location indicated that resistance to ALS inhibitors was due to an altered target site with reduced sensitivity to a broad range of ALS inhibitors. The ALS I50 values for triasulfuron, metsulfuron, chlorsulfuron, thifensulfuron, and imazethapyr were 36, 34, 92, 96, and 14 times higher, respectively, for the resistant compared to the susceptible biotype. The mechanism of resistance to quinclorac is unknown. This is the first report of high-level herbicide resistance in this weed species.

Three corn root bioassays were evaluated for detecting imazaquin in soil. Two techniques, one which utilized a cone-shaped tube as the growth container and another, a petri dish, were compared to a method that utilized a thin layer of soil between two 20 by 20 cm glass plates. Corn root growth responded logarithmically to imazaquin regardless of bioassay method. Corn was most sensitive to low imazaquin concentrations when grown using the glass plate apparatus. At a low concentration (0.5 ng/g) of imazaquin, corn root length was reduced 6% using the cone-tube, 2% using the petri dish, and 24% using the glass plate method. In contrast, the cone-tube method provided a better measure of high imazaquin concentration (200 ng/g) than the other methods.

The efficacy of current wild oat herbicides and their high cost have resulted in use rates that are less than those recommended. While acceptable weed control may be attained at less cost, this practice does not consider the potential for increased wild oat seed production. The objective of this experiment was to determine the interaction of wild oat density and reduced imazamethabenz rates on wild oat seed production in spring barley. As wild oat densities increased from 8 to 1,100 plants m−2, wild oat seed production increased from 180 to 9,950 seed m−2 without herbicide, and from 0 to 2,810 seed m−2 using 0.53 kg ai ha−1 imazamethabenz. This general pattern was modeled using a cumulative logistic function. Estimates from this model indicated that < 1 wild oat seed m−2 was produced at population densities of ≤ 20 plants at any imazamethabenz rate. Imazamethabenz rates of 0.26 kg ha−1 or greater at wild oat densities of less than approximately 190 plants m−2 did not result in wild oat seed production above the initial population density. As wild oat density increased, however, imazamethabenz rates below 0.40 kg ha−1 resulted in substantially greater wild oat seed production compared to the recommended rate.

Imazamethabenz is a selective herbicide used to control wild oat in small grains. The effects of rate, volume of carrier, and surfactant concentration on the efficacy of this herbicide in controlling wild oat were studied in field experiments. As each of the variables increased, wild oat control increased; the greatest degree of wild oat growth inhibition occurred at the highest herbicide rate, highest volume of carrier, and highest surfactant concentration.

Greenhouse and laboratory studies were conducted to determine the extent of cross-resistance of chlorsulfuron-resistant sugarbeet (CR1-B) to other herbicides that inhibit acetolactate synthase (ALS) and to determine the physiological basis of resistance. Cross-resistance to metsulfuron, imazaquin, and imazethapyr was not evident, while only marginal cross-resistance was observed to triasulfuron, DPX-L5300, and nicosulfuron. CR1-B was moderately resistant to chlorsulfuron and chlorimuron and was highly cross-resistant to thifensulfuron and primisulfuron. Further greenhouse studies demonstrated that CR1-B was not significantly injured by thifensulfuron and primisulfuron applied at or exceeding the field use rate. Studies with 14C-primisulfuron showed that differential absorption or metabolism of primisulfuron could not account for the observed resistance. ALS enzyme assays showed that the CR1-B ALS enzyme activity was 66, 26, and 13 times less sensitive to chlorsulfuron, thifensulfuron, and primisulfuron inhibition, respectively, compared to ALS enzyme extracted from sensitive sugarbeets. An altered ALS enzyme, which is less sensitive to sulfonylurea herbicide inhibition, appears to be the physiological basis of resistance.

Acetohydroxyacid synthase was discovered as the site of action of imidazolinone and sulfonylurea herbicides over 6 yr ago. In recent years, advances have been made in the understanding of this enzyme as a herbicide target site. Derivatives of both imidazolinones and sulfonylureas have yielded new herbicide chemistry. AH of the herbicides display unusual “slow-binding” behavior with the enzyme, and this behavior may help explain efficacy of the herbicides. Resistance to these herbicides has been developed through a number of different procedures, and the mechanism of resistance is through changes in sensitivity of the enzyme to the herbicides. The changes are either selective to only one class of chemistry, or broad to a number of classes of chemistry. These data support the idea that binding sites for the herbicides on the enzyme are only partially overlapping. Progress in purification of AHAS from corn includes discovery of the existence of the enzyme in monomer and oligomer aggregation states. The interaction of the enzyme with the herbicides is affected by enzyme aggregation state.

A field trial was conducted in 1988 and 1989 to confirm the efficacy of naphthalic anhydride (NA) for providing full-season protection of corn from imazethapyr applied at various times and rates. NA applied as a 1% by weight dust to corn seed caused 6% injury 2 weeks after treatment (WAT) in 1989; however, plants recovered within 6 WAT and grain yield was not affected. Imazethapyr applied to corn untreated with NA resulted in greater than 30% injury for all treatments in both years except PRE in 1988. NA reduced phytotoxicity from all imazethapyr applications in 1989 and from PPI, early POST, and 4- to 5-leaf stage (mid-POST) applications in 1988. Despite the safening effect, corn injury was still observed 6 WAT in NA-treated corn for all imazethapyr applications in both years except early POST in 1988. Higher yields were produced from NA-treated than untreated corn with imazethapyr applied PPI in both years, PRE in 1989, early POST in both years, and mid-POST in 1988. Safened corn treated PPI and early POST yielded the same as the safened corn in the control in both years. Imazethapyr applied at the 8- to 10-leaf stage caused total yield loss regardless of NA treatment. Drought conditions may have caused the lower corn injury and yield loss from imazethapyr observed in 1988 compared to 1989.

A plant response study was conducted in the greenhouse to evaluate interactions between imazamox and acifluorfen, fomesafen, or lactofen. Antagonistic interactions between imazamox and acifluorfen or fomesafen affected control of I. hederacea and A. theophrasti 21 d after treatment. Combinations of imazamox plus lactofen also antagonized control of I. hederacea. I. hederacea absorbed less 14C-imazamox when applied with nonlabeled acifluorfen, but absorption by A. theophrasti was not affected by the combination. Addition of nonlabeled lactofen did not affect absorption of imazamox in A. theophrasti or I. hederacea. Addition of acifluorfen or lactofen reduced translocation of 14C-imazamox to foliage above and below the treated leaf and the root in both A. theophrasti and I. hederacea. Antagonism of A. theophrasti control was due to reduced translocation of imazamox. Antagonism of I. hederacea control was due to reduced translocation of imazamox when applied with lactofen or reduced absorption and translocation when applied with acifluorfen.

The effects of 1.24 kg ha-1 ammonium sulfate, 5 g ae ha-1 of the isopropylamine salt of imazapyr, and air temperature of 18, 27, and 35 C at 40 and 100% relative humidity on the phytotoxicity of 35 g ae ha-1 of the ammonium salt of imazethapyr applied postemergence to pitted morningglory were evaluated. Both ammonium sulfate and imazapyr increased imazethapyr phytotoxicity to pitted morningglory. Ammonium sulfate enhanced imazethapyr phytotoxicity the most at 40% whereas imazapyr was most effective at 100% relative humidity. Imazethapyr phytotoxicity was enhanced more by the combination of ammonium sulfate and imazapyr than with either alone regardless of relative humidity. Variations in temperature had little effect on phytotoxicity.

‘Cargill 921′, ‘Great Lakes 422′, ‘Northrup King 9410′, ‘Pioneer 3901′, ‘Pioneer 3737′, and ‘Stauffer 5650’ corn hybrids were tested in the greenhouse for imazaquin tolerance. Imazaquin rates that reduced shoot growth 50%, when compared to the untreated hybrid check, ranged from 17 to 50 g/ha. When averaged together, the three most tolerant hybrids (Cargill 921, Pioneer 3901, and Great Lakes 422) were approximately one-half as sensitive to imazaquin as the three least tolerant hybrids (Northrup King 9410, Pioneer 3737, and Stauffer 5650). Studies were conducted to determine if the observed differential tolerance was caused by differences in acetolactate synthase (ALS, EC 4.1.3.18) levels and sensitivity of ALS to imazaquin. Differential imazaquin uptake, translocation, and/or metabolism were also studied as a basis for the tolerance range as was seed size and seedling growth. There were differences among hybrids in the physiological and growth parameters studied; however, these differences did not correlate with imazaquin tolerance. None of the factors studied could alone account for the differences in imazaquin tolerance.

Field and laboratory studies were conducted to determine if differences existed in pinto bean varietal tolerance to postemergence application of imazethapyr under field conditions; if differences in tolerance were due to differential acetolactate synthase enzyme sensitivity or differences in 14C-imazethapyr absorption, translocation, and metabolism; and the heritability of imazethapyr tolerance in pinto bean. All rates of imazethapyr injured Olathe, Sierra, UI-114, P89405, Aztec, and P90570 pinto bean varieties 7 d after treatment in 1991 and 1992, except 53 g ai ha−1 of imazethapyr applied to Sierra pinto bean in 1991. Olathe was injured more than other varieties in 1991, and physiological maturity of Olathe was delayed more than Sierra in 1991 and 1992. Seed yields of all varieties were not reduced in 1991, and only P90570 had reduced seed yields from 53 g ha−1 of imazethapyr in 1992. Differential sensitivity of the acetolactate synthase enzyme to imazethapyr was not the mechanism of differential varietal response. Olathe pinto bean absorbed and translocated 1.4 and 1.3 times more 14C-imazethapyr, respectively, than Sierra pinto bean 24 h after application. No differences in 14C-imazethapyr metabolism were detected between Olathe and Sierra pinto bean. Broad heritability of imazethapyr tolerance in pinto bean was calculated to be 0.85. The number of genes controlling the inheritance of imazethapyr tolerance in pinto bean was greater than one.

In vitro acetolactate synthase (ALS) activity from three commercial imidazolinone-resistant corn hybrids (ICI 8692 IT, Pioneer 3751 IR, and Ciba 4393 IMR) was compared to imidazolinone-sensitive isogenic hybrid controls for sensitivity to 11 herbicides representing four classes of ALS-inhibiting herbicide chemistry. Acetolactate synthase activity from Pioneer IR and Ciba IMR was cross-resistant to all four classes of ALS inhibitors, ranging from 48- to 5,000-fold. The ICI IT hybrid displayed only four- to eightfold resistance to the six imidazolinone herbicides and the pyrimidinylthiobenzoate herbicide, pyrithiobac, but no cross-resistance to the sulfonylurea and triazolopyrimidine sulfonanilide herbicides. The four- to eightfold enzyme resistance to imidazolinone herbicides provides whole-plant resistance; however, the sevenfold enzyme resistance to pyrithiobac was insufficient to afford whole-plant protection to a field application rate of the herbicide. A second imidazolinone-specific resistance allele, XI-12, currently under commercial development, was examined for the level of dominance at the enzyme level. In the heterozygous state, imazethapyr resistance was fivefold, compared to 250-fold in the homozygous condition, indicating XI-12 is a semidominant trait. No cross-resistance to nicosulfuron or primisulfuron was observed in the heterozygous XI-12 hybrid extracts nor to nicosulfuron in the XI-12 homozygote; however, a fivefold resistance to primisulfuron was detected in the XI-12 homozygote.

A naturally occurring prickly lettuce biotype resistant to a 5:1 formulated mixture of chlorsulfuron:metsulfuron (DPX-G8311) was identified in a no-till winter wheat field near Lewiston, ID, in April, 1987. Field and greenhouse studies were established to evaluate its resistance to other sulfonylureas, imidazolinones, and herbicides with alternate sites of action. The resistant biotype resisted eight sulfonylurea herbicides; resisted the imidazolinone herbicides, imazapyr and imazethypyr, but not imazaquin; and resisted no other herbicides included in the studies. The resistant biotype was identified in seven of nine fields on the farm where it was discovered.