Amaranthus species are problematic weeds in snap bean production systems. They reduce crop yields, and their stem fragments contaminate harvested pods. Knowledge of snap bean tolerance to different preemergence herbicides is limited; however, knowing this tolerance is essential for planning a reliable weed management system, breeding herbicide-tolerant cultivars, and registering herbicides for use on minor crops such as snap bean. Field trials were conducted in 2021 and 2022 to determine the tolerance of eight snap bean cultivars to preemergence herbicides with activity on Amaranthus species, including dimethenamid-P, flumioxazin, lactofen, metribuzin, saflufenacil, and sulfentrazone. Snap bean plant density (number of plants per square meter), plant biomass (grams per plant), and canopy biomass (grams per square meter) 21 d after treatment were used to assess crop tolerance to a range of herbicide rates. Linear mixed-effects regression models were fitted to quantify the relationships between preemergence herbicide rate and snap bean cultivar tolerance. Results indicated a high margin of crop safety with dimethenamid-P and lactofen for weed control in snap bean, and a low margin of crop safety with metribuzin and saflufenacil. Results indicated differential cultivar tolerance to flumioxazin and sulfentrazone, which could be driven by genetic variability among cultivars.

Pink purslane is often ranked as one of the most troublesome weeds in vegetable production systems in Georgia. Pink purslane encroachment along field edges and in-field of agronomic crops has recently increased. Postemergence herbicides are an effective component of agronomic crop weed management. However, little research has addressed pink purslane control in agronomic crops. Therefore, greenhouse and field studies were conducted from 2022 to 2023 in Tifton, Georgia, to evaluate the response of pink purslane to postemergence herbicides commonly used in agronomic crops. Greenhouse screening provided preliminary evidence whereby 13 of the 21 postemergence herbicides evaluated provided ≥80% aboveground biomass reductions. These 13 herbicides were then used for field studies. Results from the field studies, pooled across two locations, indicated that only three of the 13 herbicides provided aboveground biomass reductions of ≥70% compared to the nontreated control. Those herbicides included atrazine at 1,682 g ai ha−1, glufosinate at 656 g ai ha−1, and lactofen at 219 g ai ha−1 with 79%, 70%, and 83% biomass reduction, respectively (P < 0.05). This research suggests that many of the postemergence herbicides used on agronomic crops will not effectively control pink purslane. Thus, when trying to manage pink purslane with postemergence herbicides in agronomic crops, growers should plant crops or cultivars that are tolerant of either atrazine, glufosinate, lactofen, or a combination of these.

Herbicides that inhibit protoporphyrinogen oxidase (PPO) are used in more than 40 agronomic and specialty crops across Georgia to manage weeds through residual and postemergence (POST) control. In 2017, a population of Palmer amaranth exhibiting reduced sensitivity to POST applications of PPO-inhibiting herbicides was identified by the University of Georgia. Seed were collected from the site along with a known sensitive population; distance between the samples was 200 m, increasing the likelihood of similar environmental and genetic characteristics. To quantify sensitivity for both preemergence (PRE) and POST uses, 21 greenhouse dose-response assessments were conducted from 2017 to 2022. After conducting initial rate-response studies, 13 doses per herbicide were chosen for the POST experiment; field use rates of fomesafen (420 g ai ha−1), lactofen (219 g ai ha−1), acifluorfen (420 g ai ha−1), and trifludimoxazin (25 g ai ha−1) ranging from 0× to 4× the field use rate for the susceptible population, and 0× to 40× for the suspect population were applied. Herbicide treatments included adjuvants and were applied to plants 8 to 10 cm in height. Relative resistance factors (RRFs) were calculated for control ratings, mortality, and biomass, and ranged from 105 to 318, 36 to 1,477, 215 to 316, and 9 to 49 for fomesafen, lactofen, acifluorfen, and trifludimoxazin, respectively. In the PRE experiment, herbicide applications included five to nine doses of fomesafen (1× = 210 g ai ha−1), flumioxazin (1× = 57 g ai ha−1), oxyfluorfen (1× = 561 g ai ha−1), and trifludimoxazin (1× = 38 g ai ha−1); doses ranged from 0× to 6× for the suspect population and 0× to 2× for the susceptible population. Visual control, mortality, and biomass RRFs ranged from 3 to 5 for fomesafen, 21 to 31 for flumioxazin, 6 to 22 for oxyfluorfen, and 8 to 38 for trifludimoxazin. Results confirm that a Georgia Palmer amaranth population is resistant to PPO-inhibiting herbicides applied both PRE and POST.

The continued dispersal of Palmer amaranth can impose detrimental impacts on cropping systems in Wisconsin. Our objective was to characterize the response of a recently introduced Palmer amaranth accession in southern Wisconsin to postemergence (POST) and preemergence (PRE) herbicides commonly used in corn and soybean. Greenhouse experiments were conducted with the Wisconsin putative herbicide-resistant accession (BRO) and two additional control accessions from Nebraska, a glyphosate-resistant (KEI2) and a glyphosate-susceptible (KEI3) accession. POST treatments were 2,4-D, atrazine, dicamba, glufosinate, glyphosate, imazethapyr, lactofen, and mesotrione at 1X and 3X label rates. PRE treatments were atrazine, mesotrione, metribuzin, S-metolachlor, and sulfentrazone at 0.5X, 1X, and 3X label rates. Plant survival of each accession was ≥63% after exposure to imazethapyr POST 3X rate. Survival of BRO and KEI2 was 44% (±13) and 50% (±13), respectively, after exposure to atrazine POST 3X rate. Survival of BRO was 69% (±12) after exposure to glyphosate POST 1X rate, whereas survival of KEI2 was 44% (±13) after exposure to glyphosate POST 3X rate. After exposure to 2,4-D POST 1X rate, KEI2 and KEI3 survival was 38% (±13) and 50% (±13), respectively. Survival of all accessions was ≤31% after exposure to 2,4-D POST 3X rate or dicamba, glufosinate, lactofen, and mesotrione POST at either rate. Plant density reduction of KEI2 was 77% (±13) after exposure to atrazine PRE 1X rate, whereas density reduction of BRO was 56% (±13) after exposure to atrazine PRE 3X rate. Plant density reduction of all accessions was ≥94% after exposure to mesotrione PRE 1X and 3X rates or metribuzin, S-metolachlor, and sulfentrazone PRE at either rate. Our results suggest that each accession is resistant (≥50% survival) to imazethapyr POST, that BRO and KEI2 are resistant to atrazine and glyphosate POST, and that KEI2 and KEI3 are resistant to 2,4-D POST. The recently introduced BRO accession exhibited multiple resistance to imazethapyr, atrazine, and glyphosate POST. In addition, atrazine PRE was ineffective for BRO control, suggesting that diversified resistance management strategies will be critical for its effective management.

Rapid vegetative growth and adverse application conditions are common factors leading to the failure of postemergence herbicides on Palmer amaranth. A sequential herbicide application, or respray, is often necessary to control weeds that have survived the initial herbicide application to protect crop yield and minimize weed seed production. The optimum timing after the initial application and the most effective herbicide for control of Palmer amaranth has not been characterized. The objectives of these experiments were to determine the optimum herbicide for treating Palmer amaranth regrowth, the optimum timing for each of those herbicides, and how the initial failed herbicide might affect efficacy of a second herbicide application. Bare ground field experiments were performed in 2017 and 2018 in which glufosinate or fomesafen herbicide failure was induced on Palmer amaranth plants that were 30 cm in height. Respray treatments of glufosinate, fomesafen, lactofen, 2,4-D, and dicamba were applied once at timings of 4 to 5 d, 7 d, or 11 d after the initial spray application. Nearly all herbicide treatment and timing combinations increased control by at least 13 percentage points compared to no respray herbicide treatment. Regardless of initial herbicide, glufosinate applied as a respray treatment was the most consistent and efficacious with up to 97% control. The specific herbicide used in the second application impacted final weed control more so than timing of the respray application. For instance, control by glufosinate respray treatments was 10 to 18 percentage points greater than control from lactofen respray treatments, whereas control decreased by 3 percentage points when respray applications of any herbicide were made 11 d after initial application of glufosinate compared to 4 to 5 and 7 d after initial application of glufosinate. In the event of failure to control Palmer amaranth with glufosinate or fomesafen, glufosinate should be applied in order to maximize control.

Palmer amaranth is the latest pigweed species documented in Connecticut; it was identified there in 2019. In a single-dose experiment, the Connecticut Palmer amaranth biotype survived the field-use rates of glyphosate (840 g ae ha−1) and imazaquin (137 g ai ha−1) herbicides applied separately. Additional experiments were conducted to (1) determine the level of resistance to glyphosate and acetolactate synthase (ALS) inhibitors in the Connecticut-resistant (CT-Res) biotype using whole-plant dose-response bioassays, and (2) evaluate the response of the CT-Res biotype to POST herbicides commonly used in Connecticut cropping systems. Based on the effective dose required for 90% control (ED90), the CT-Res biotype was 10-fold resistant to glyphosate when compared with the Kansas-susceptible (KS-Sus) biotype. Furthermore, the CT-Res biotype was highly resistant to ALS-inhibitor herbicides; only 18% control was achieved with 2,196 g ai ha−1 imazaquin. The CT-Res biotype was also cross-resistant to other ALS-inhibitor herbicides, including chlorimuron-ethyl (13.1 g ai ha−1), halosulfuron-methyl (70 g ai ha−1), and sulfometuron-methyl (392 g ai ha−1). The CT-Res Palmer amaranth was controlled 75% to 100% at 21 d after treatment (DAT) with POST applications of 2,4-D (386 g ae ha−1), carfentrazone-ethyl (34 g ai ha−1), clopyralid (280 g ae ha−1), dicamba (280 g ae ha−1), glufosinate (595 g ai ha−1), lactofen (220 g ai ha−1), oxyfluorfen (1,121g ai ha−1), and mesotrione (105 g ai ha−1) herbicides. Atrazine (2,240 g ai ha−1) controlled the CT-Res biotype only 52%, suggesting the biotype is resistant to this herbicide as well. Here we report the first case of Palmer amaranth from Connecticut with multiple resistance to glyphosate and ALS inhibitors. Growers should proactively use all available weed control tactics, including the use of effective PRE and alternative POST herbicides (tested in this study), for effective control of the CT-Res biotype.

Glyphosate-resistant (GR) Palmer amaranth is a troublesome weed that can emerge throughout the soybean growing season in Nebraska and several other regions of the United States. Late-emerging Palmer amaranth plants can produce seeds, thus replenishing the soil seedbank. The objectives of this study were to evaluate single or sequential applications of labeled POST herbicides such as acifluorfen, dicamba, a fomesafen and fluthiacet-methyl premix, glyphosate, and lactofen on GR Palmer amaranth control, density, biomass, seed production, and seed viability, as well as grain yield of dicamba- and glyphosate-resistant (DGR) soybean. Field experiments were conducted in a grower’s field infested with GR Palmer amaranth near Carleton, NE, in 2018 and 2019, with no PRE herbicide applied. Acifluorfen, dicamba, a premix of fomesafen and fluthiacet-methyl, glyphosate, or lactofen were applied POST in single or sequential applications between the V4 and R6 soybean growth stages, with timings based on product labels. Dicamba applied at V4 or in sequential applications at V4 followed by R1 or R3 controlled GR Palmer amaranth 91% to 100% at soybean harvest, reduced Palmer amaranth density to as low as 2 or fewer plants m−2, reduced seed production to 557 to 2,911 seeds per female plant, and resulted in the highest soybean yield during both years of the study. Sequential applications of acifluorfen, fomesafen and fluthiacet premix, or lactofen were not as effective as dicamba for GR Palmer amaranth control; however, they reduced seed production similar to dicamba. On the basis of the results of this study, we conclude that dicamba was effective for controlling GR Palmer amaranth and reduced density, biomass, and seed production without DGR soybean injury. Herbicides evaluated in this study had no effect on Palmer amaranth seed viability.

During the 2017 to 2019 growing seasons, samples of waterhemp and Palmer amaranth that had reportedly survived field-rate applications of protoporphyrinogen oxidase (PPO)–inhibiting herbicides were collected from the American Midwest and tested for target-site mutations known at the time to confer resistance. Target-site resistance was identified in nearly all (135 of 145) tested common waterhemp populations but in only 8 of 13 Palmer amaranth populations. Follow-up research on one population of Palmer amaranth (W-8), which tested negative for all such mutations, confirmed it was resistant to lactofen, with a magnitude of resistance comparable to that conferred by the ΔG210 PPO2 mutation. Gene sequences from both isoforms of PPO (PPO1 and PPO2) were compared between W-8 and known PPO inhibitor–sensitive sequence. A glycine-to-alanine substitution at the 399th amino acid position (G399A) of PPO2, recently identified to reduce target-site herbicide sensitivity, was observed in a subset of resistant W-8 plants. Because no missense mutation completely delimited resistant and sensitive sequences, we initially suspected the presence of a secondary, non-target-site resistance mechanism in this population. To isolate G399A, a segregating F2 population was produced and screened with a delimiting rate of lactofen. χ2 goodness-of-fit analysis of dead/alive ratings indicated single-locus inheritance of resistance in the F2 population, and molecular markers for the W-8 parental PPO2 coding region co-segregated tightly, but not perfectly, with resistance. More research is needed to fully characterize Palmer amaranth PPO inhibitor–resistance mechanisms, which appear to be more diverse than those found in common waterhemp.

Failure to control Palmer amaranth with glyphosate and protoporphyrinogen IX oxidase (PPO)-inhibitor herbicides was reported across southwestern Nebraska in 2017. The objectives of this study were to 1) confirm and 2) validate glyphosate and PPO-inhibitor (fomesafen and lactofen) resistance in 51 Palmer amaranth accessions from southwestern Nebraska using genotypic and whole-plant phenotypic assay correlations and cluster analysis, and 3) determine which agronomic practices might be influencing glyphosate resistance in Palmer amaranth accessions in that location. Based on genotypic assay, 88% of 51 accessions contained at least one individual with amplification (>2 copies) of the 5-enolypyruvyl-shikimate-3-phosphate synthase (EPSPS) gene, which confers glyphosate resistance; and/or a mutation in the PPX2 gene, either ΔG210 or R128G, which endows PPO-inhibitor resistance in Palmer amaranth. Cluster analysis and high correlation (0.83) between genotypic and phenotypic assays demonstrated that EPSPS gene amplification is the main glyphosate resistance mechanism in Palmer amaranth accessions from southwestern Nebraska. In contrast, there was poor association between genotypic and phenotypic responses for PPO-inhibitor resistance, which was attributed to segregation for PPO-inhibitor resistance within these accessions and/or the methodology that was adopted herein. Genotypic assays can expedite the process of confirming known glyphosate and PPO-inhibitor resistance mechanisms in Palmer amaranth from southwestern Nebraska and other locations. Phenotypic assays are also a robust method for confirming glyphosate resistance but not necessarily PPO-inhibitor resistance in Palmer amaranth. Moreover, random forest analysis of glyphosate resistance in Palmer amaranth indicated that EPSPS gene amplification, county, and current and previous crops are the main factors influencing glyphosate resistance within that geographic area. Most glyphosate-susceptible Palmer amaranth accessions were found in a few counties in areas with high crop diversity. Results presented here confirm the spread of glyphosate resistance and PPO-inhibitor resistance in Palmer amaranth accessions from southwestern Nebraska and demonstrate that less diverse cropping systems are an important driver of herbicide resistance evolution in Palmer amaranth.

Foliar herbicide applications to waterhemp can result in inadequate control, leading to subsequent regrowth that often necessitates a second herbicide application to prevent crop interference and seed production. The most effective herbicides and application timings are unknown in situations where waterhemp has regrown from previous injury, such as failed applications of glufosinate or fomesafen. The objective of this research was to determine the optimum combination of herbicide and time from the first failed herbicide application to a sequential herbicide application for control of waterhemp regrowth. Reduced rates of either glufosinate or fomesafen were applied to 30-cm waterhemp plants to mimic failure of the initial herbicide application in separate bare-ground experiments. Respray treatments of glufosinate, fomesafen, lactofen, 2,4-D, or dicamba were applied 3, 7, or 11 d after the initial application. Glufosinate and fomesafen as respray treatments resulted in 90% to 100% control of waterhemp regardless of application timing following a failed glufosinate application. After a failed application of fomesafen, applying glufosinate or 2,4-D resulted in 87% to 99% control of waterhemp. Waterhemp control with fomesafen and lactofen was 13% to 21% greater, respectively, when those treatments followed glufosinate compared with fomesafen as the initial herbicides. On the basis of these results, glufosinate and fomesafen should be used for respray situations after inadequate control from glufosinate; and 2,4-D or glufosinate should be used for respray situations following inadequate control from fomesafen where crop tolerance and herbicide product labels allow. Although glufosinate followed by glufosinate was very effective for controlling waterhemp regrowth, caution should be exercised to avoid sequential application of herbicide with the same site of action.

Wild poinsettia (Euphorbia heterophylla L.) is a troublesome broadleaf weed in grain production areas in South America. Herbicide resistance to multiple sites of action has been documented in this species, including protoporphyrinogen oxidase (PPO) inhibitors. We investigated the physiological and molecular bases for PPO-inhibitor resistance in a E. heterophylla population (RPPO) from Southern Brazil. Whole-plant dose–response experiments revealed a cross-resistance profile to three different chemical groups of PPO inhibitors. Based on dose–response parameters, RPPO was resistant to lactofen (47.7-fold), saflufenacil (8.6-fold), and pyraflufen-ethyl (3.5-fold). Twenty-four hours after lactofen treatment (120 g ha−1) POST, RPPO accumulated 27 times less protoporphyrin than the susceptible population (SPPO). In addition, RPPO generated 5 and 4.5 times less hydrogen peroxide and superoxide than SPPO, respectively. The chloroplast PPO (PPO1) sequences were identical between the two populations, whereas 35 single-nucleotide polymorphisms were found for the mitochondrial PPO (PPO2). Based on protein homology modeling, the Arg-128-Leu (homologous to Arg-98-Leu in common ragweed [Ambrosia artemisiifolia L.] was the only one located near the catalytic site, also in a conserved region of PPO2. The cytochrome P450 monooxygenase inhibitor malathion did not reverse resistance to lactofen in RPPO, and both populations showed similar levels of PPO1 and PPO2 expression, suggesting that metabolic resistance and PPO overexpression are unlikely. This is the first report of an Arg-128-Leu mutation in PPO2 conferring cross-resistance to PPO inhibitors in E. heterophylla.

Herbicide applications performed with pulse width modulation (PWM) sprayers to deliver specific spray droplet sizes could maintain product efficacy, minimize potential off-target movement, and increase flexibility in field operations. Given the continuous expansion of herbicide-resistant Palmer amaranth populations across the southern and midwestern United States, efficacious and cost-effective means of application are needed to maximize Palmer amaranth control. Experiments were conducted in two locations in Mississippi (2016, 2017, and 2018) and one location in Nebraska (2016 and 2017) for a total of 7 site-years. The objective of this study was to evaluate the influence of a range of spray droplet sizes [150 (Fine) to 900 μm (Ultra Coarse)] on lactofen and acifluorfen efficacy for Palmer amaranth control. The results of this research indicated that spray droplet size did not influence lactofen efficacy on Palmer amaranth. Palmer amaranth control and percent dry-biomass reduction remained consistent with lactofen applied within the aforementioned droplet size range. Therefore, larger spray droplets should be used as part of a drift mitigation approach. In contrast, acifluorfen application with 300-μm (Medium) spray droplets provided the greatest Palmer amaranth control. Although percent biomass reduction was numerically greater with 300-μm (Medium) droplets, results did not differ with respect to spray droplet size, possibly as a result of initial plant injury, causing weight loss, followed by regrowth. Overall, 900-μm (Ultra Coarse) droplets could be used effectively without compromising lactofen efficacy on Palmer amaranth, and 300-μm (Medium) droplets should be used to achieve maximum Palmer amaranth control with acifluorfen.

Resistance to protoporphyrinogen oxidase (PPO) inhibitors was first observed in waterhemp in 2001 and was conferred by the deletion of a glycine residue at the 210th position (ΔGly-210) of the PPO enzyme. PPO-inhibitor resistance in Palmer amaranth was first observed in 2011, 10 years later. The objectives of this study were to directly compare PPO inhibitor responses in plants of both species with or without the ΔGly-210 mutation. Using greenhouse experiments, early (EPOST) and late (LPOST) postemergence dose responses using lactofen and fomesafen, and preemergence (PRE) dose responses using fomesafen and flumioxazin, were obtained for a sensitive and resistant population each of waterhemp and Palmer amaranth. An additional spray study confirmed each sensitive population used in the dose responses was representative of its respective species, with regards to PPO-inhibitor sensitivity. When treated at either POST timing, Palmer amaranth was more tolerant than waterhemp, and the ΔGly-210 mutation provided greater resistance in Palmer amaranth (48-fold to >3,440-fold, depending on timing and herbicide) than in waterhemp (31-fold to 123-fold). The level of tolerance in Palmer amaranth was striking; the sensitive Palmer amaranth population treated LPOST survived as well or better than the resistant waterhemp population treated EPOST. With PRE applications, response differences both between species and between resistant and sensitive populations generally were less pronounced, relative to POST applications. Collectively, this research indicates Palmer amaranth tolerance to POST-applied PPO inhibitors could have initially slowed (relative to waterhemp) evolution of resistance to these herbicides, and resistant and sensitive populations of both species are more likely to be effectively controlled with PRE rather than POST applications.

Studies to evaluate the effect of application time of day (TOD) and protoporphyrinogen IX oxidase (PPO)-inhibiting herbicide–resistant Palmer amaranth on the efficacy of commonly used herbicides was conducted in Tennessee in 2017 and 2018. Treatments of fomesafen, lactofen, acifluorfen, paraquat, glufosinate, glufosinate plus fomesafen, paraquat plus fomesafen, and paraquat plus metribuzin were applied to PPO-resistant (PPO-R) and PPO-susceptible (PPO-S) Palmer amaranth at sunrise and midday. Control of Palmer amaranth with acifluorfen, glufosinate, and glufosinate plus fomesafen was greater with the midday application. However, control of Palmer amaranth with paraquat-based treatments was greater with the sunrise application. TOD effects on PPO-inhibiting herbicides and paraquat-based treatments were more prominent for the PPO-R Palmer amaranth biotype. The TOD effect observed when applying glufosinate in early morning hours on PPO-S Palmer amaranth can be minimized by adding fomesafen to the tank mix. However, this strategy did not provide consistent performance on PPO-R Palmer amaranth. The percentages of living Palmer amaranth plants and control were greater when paraquat plus metribuzin was applied to both biotypes. These results highlight the necessity of at least two effective herbicide sites of action for POST applications intended for controlling PPO-R Palmer amaranth. In addition, the timing of herbicide applications can affect their activity in both PPO-R and PPO-S Palmer amaranth populations.

Diphenyl ether herbicides are commonly applied POST in soybean to control weeds late in the growing season that have not been controlled by other previous weed management tactics. These “rescue” applications can occur during reproductive soybean growth. The effect of these herbicides on the developing flowers and pods is not known. Field research studies were conducted over 3 yr to determine how soybean flowers and developing pods respond to fomesafen, acifluorfen, and lactofen when applied at R1, R3, and R5 growth stages. Flower and pod counts in the nontreated check showed an increase (17.1, 5.8, and 2.21 at R1, R3, and R5 stage, respectively) and were statistically the same as the herbicide treatments 1 wk after treatment. Fomesafen, acifluorfen, and lactofen applied at 395, 420, and 219 g ai ha–1 at R1, R3, and R5 stage had no negative impact on soybean flowers and developing pods when compared to the nontreated check. No significant differences were observed in soybean yield between any treatments in all site-years of the study.

In the rapid response (RR) biotype of glyphosate-resistant (GR) giant ragweed (Ambrosia trifida L.), exposure to glyphosate elicits H2O2 production in mature leaves, resulting in foliage loss and reduced glyphosate translocation. When glyphosate is applied with POST herbicides intended to improve control of A. trifida, the RR to glyphosate has the propensity to antagonize these herbicide combinations. This research documents how transient changes in air temperature, soil moisture, and light intensity during a 6-d period surrounding herbicide application regulate induction of the RR and the effect on POST herbicide interactions with glyphosate. Air temperature had the greatest influence on H2O2 accumulation in leaf disks following treatment with glyphosate, as plants at 30 C produced more than twice the amount of H2O2 at 2.5 h after treatment compared with 10 C. Plants under field capacity conditions accumulated nearly 50% more H2O2 than those at one-third field capacity, while those under no shade had only 18% more H2O2 compared with those in a shaded environment. Despite these initial results, dry weight reduction at 21 d after treatment never differed by more than 8% between levels of environmental factors, thus indicating a negligible influence on glyphosate efficacy. The magnitude of glyphosate-induced antagonism was generally greater at 30 C (12% to 21% less than expected control) versus 10 C (11% to 16%) on atrazine, cloransulam, dicamba, and topramezone and was greater at field capacity (20% to 24%) versus one-third field capacity (11% to 15%) on cloransulam and topramezone. These results indicate air temperatures and soil moisture levels conducive to optimal plant growth accelerate the RR to glyphosate, thereby increasing the likelihood of glyphosate-induced antagonism on several translocated herbicides.

Glyphosate application to the rapid-response (RR) biotype of glyphosate-resistant (GR) giant ragweed ensues in loss of foliage via rapid tissue death, thereby reducing glyphosate translocation. Experiments were performed to determine if this GR response, in contrast to a non-rapid response (NRR) GR biotype, results in antagonism of the selective herbicides atrazine, cloransulam, dicamba, lactofen, and topramezone. Application of glyphosate at 1,680 g ae ha–1 in the greenhouse resulted in antagonism between all five selective herbicides for the RR biotype, whereas glyphosate applied at 420 g ha–1 was antagonistic only for cloransulam. Application of selective herbicides 2 d prior to glyphosate treatment avoided the antagonism observed in the RR biotype. In the field, glyphosate mixtures with dicamba and topramezone were antagonistic on the RR biotype across both 2015 and 2016 field seasons. Thus, the RR effectively reduces glyphosate efficacy but also has potential to diminish the activity of glyphosate mixtures with selective herbicides, and the degree of antagonism between these mixtures escalates at increasing glyphosate rates.

A 2,4-D-resistant tall waterhemp population (FS) from Nebraska was evaluated for resistance to other TIR1 auxin receptor herbicides and to herbicides having alternative mechanisms of action using greenhouse bioassays and genetic markers. Atrazine, imazethapyr, lactofen, mesotrione, glufosinate, and glyphosate were applied in a single-dose bioassay, and tissue was collected from marked plants for genetic analysis. The FS population was not injured by atrazine or by imazethapyr. Approximately 50% of the plants survived lactofen and were actively growing 28 d after treatment. The population was susceptible to mesotrione, glufosinate, and glyphosate. Ametryn, chlorimuron-ethyl, 2,4-D, aminocyclopyraclor, aminopyralid, and picloram were applied in dose–response studies. The FS population was sensitive to ametryn, and the Ser-264-Gly substitution in the D1 protein was not detected, suggesting the lack of response to atrazine is not due to a target-site mutation. The FS population exhibited less than 50% injury to chlorimuron-ethyl at application rates 20 times the labeled use rate. The Ser-653-Asn acetolactate synthase (ALS) substitution, which confers resistance to imidazolinone herbicides, was present in the FS population. However, this does not explain the lack of response to the sulfonylurea herbicide, chlorimuron-ethyl. Sequencing of a portion of the PPX2L gene did not show the ΔG210 mutation that confers resistance to protoporphyrinogen oxidase–inhibiting herbicides, suggesting that other factors were responsible for waterhemp survival after lactofen application. The FS population was confirmed to be at least 30-fold resistant to 2,4-D relative to the susceptible populations. In addition, it was at least 3-fold less sensitive to aminopyralid and picloram, two other TIR1 auxin receptor herbicides, than the 2,4-D-susceptible populations were. These data indicated that the FS population contains both target and non–target site mechanisms conferring resistance to herbicides spanning at least three mechanisms of action: TIR1 auxin receptors, ALS inhibitors, and photosystem II inhibitors.

The widespread occurrence of Palmer amaranth resistant to acetolactate synthase inhibitors and/or glyphosate led to the increased use of protoporphyrinogen oxidase (PPO)-inhibiting herbicides. This research aimed to: (1) evaluate the efficacy of foliar-applied fomesafen to Palmer amaranth, (2) evaluate cross-resistance to foliar PPO inhibitors and efficacy of foliar herbicides with different mechanisms of action, (3) survey the occurrence of the PPO Gly-210 deletion mutation among PPO inhibitor–resistant Palmer amaranth, (4) identify other PPO target-site mutations in resistant individuals, and (5) determine the resistance level in resistant accessions with or without the PPO Gly-210 deletion. Seedlings were sprayed with fomesafen (263 gaiha−1), dicamba (280 gaiha−1), glyphosate (870 gaiha−1), glufosinate (549 g ai ha−1), and trifloxysulfuron (7.84 gaiha−1). Selected fomesafen-resistant accessions were sprayed with other foliar-applied PPO herbicides. Mortality and injury were evaluated 21 d after treatment (DAT). The PPX2L gene of resistant and susceptible plants from a selected accession was sequenced. The majority (70%) of samples from putative PPO-resistant populations in 2015 were confirmed resistant to foliar-applied fomesafen. The efficacy of other foliar PPO herbicides on fomesafen-resistant accessions was saflufenacil>acifluorfen=flumioxazin>carfentrazone=lactofen>pyraflufen-ethyl>fomesafen>fluthiacet-methyl. With small seedlings, cross-resistance occurred with all foliar-applied PPO herbicides except saflufenacil (i.e., 25% with acifluorfen, 42% with flumioxazin). Thirty-two percent of PPO-resistant accessions were multiple resistant to glyphosate and trifloxysulfuron. Resistance to PPO herbicides in Palmer amaranth occurred in at least 13 counties in Arkansas. Of 316 fomesafen survivors tested, 55% carried the PPO Gly-210 deletion reported previously in common waterhemp. The PPO gene (PPX2L) in one accession (15CRI-B), which did not encode the Gly-210 deletion, encoded an Arg-128-Gly substitution. The 50% growth reduction values for fomesafen in accessions with Gly-210 deletion were 8- to 15-fold higher than that of a susceptible population, and 3- to 10-fold higher in accessions without the Gly-210 deletion.

Quizalofop controlled 2- to 3-leaf and 5- to 6-leaf red rice better than fluazifop-P, haloxyfop, or sethoxydim applied alone. Red rice control increased when acifluorfen was tank mixed with haloxyfop, fluazifop-P, or sethoxydim. Antagonism was most severe when imazaquin was tank mixed with any of the grass herbicides. The efficacy of sethoxydim, fluazifop-P, and haloxyfop was reduced when applied with chlorimuron or bentazon. In greenhouse experiments, all of the grass herbicides, except for fenoxaprop, reduced fresh weight of red rice 71% or more. Based on fresh weight reduction, acifluorfen, fomesafen, and lactofen only reduced the activity of fluazifop-P, while imazaquin decreased the activity of all grass herbicides.