The U.S. Department of Agriculture–Agricultural Research Service (USDA-ARS) has been a leader in weed science research covering topics ranging from the development and use of integrated weed management (IWM) tactics to basic mechanistic studies, including biotic resistance of desirable plant communities and herbicide resistance. ARS weed scientists have worked in agricultural and natural ecosystems, including agronomic and horticultural crops, pastures, forests, wild lands, aquatic habitats, wetlands, and riparian areas. Through strong partnerships with academia, state agencies, private industry, and numerous federal programs, ARS weed scientists have made contributions to discoveries in the newest fields of robotics and genetics, as well as the traditional and fundamental subjects of weed–crop competition and physiology and integration of weed control tactics and practices. Weed science at ARS is often overshadowed by other research topics; thus, few are aware of the long history of ARS weed science and its important contributions. This review is the result of a symposium held at the Weed Science Society of America’s 62nd Annual Meeting in 2022 that included 10 separate presentations in a virtual Weed Science Webinar Series. The overarching themes of management tactics (IWM, biological control, and automation), basic mechanisms (competition, invasive plant genetics, and herbicide resistance), and ecosystem impacts (invasive plant spread, climate change, conservation, and restoration) represent core ARS weed science research that is dynamic and efficacious and has been a significant component of the agency’s national and international efforts. This review highlights current studies and future directions that exemplify the science and collaborative relationships both within and outside ARS. Given the constraints of weeds and invasive plants on all aspects of food, feed, and fiber systems, there is an acknowledged need to face new challenges, including agriculture and natural resources sustainability, economic resilience and reliability, and societal health and well-being.

Weeds and invasive plants know no borders and have collectively impacted many ecosystems worldwide, including croplands, forests, grasslands, rangelands, wetlands, and riparian areas. Losses continue to mount, affecting yield and productivity, species diversity, and ecosystem services, with both short- and long-term repercussions on the sustainability of plant and animal communities and the livelihoods of many. New and emerging invasive plants, along with many of the most intractable weeds, have undermined even the best control efforts, serving as a reminder of the constant need for improvements in science, application, and technology. One of the main reasons for the success of weeds and invasive plants is their ability to adapt to abiotic and biotic conditions, and research suggests that this will continue with minimal change.

Multiple resistance to glyphosate, sethoxydim, and paraquat was previously confirmed in two Italian ryegrass [Lolium perenne L. ssp. multiflorum (Lam.) Husnot] populations, MR1 and MR2, in northern California. Preliminary greenhouse studies revealed that both populations were also resistant to imazamox and mesosulfuron, both of which are acetolactate synthase (ALS)-inhibiting herbicides. In this study, three subpopulations, MR1-A (from seed of MR1 plants that survived a 16X rate of sethoxydim), MR1-P (from seed of MR1 plants that survived a 2X rate of paraquat), and MR2 (from seed of MR2 plants that survived a 16X rate of sethoxydim), were investigated to determine the resistance level to imazamox and mesosulfuron, evaluate other herbicide options for the control of these multiple resistant L. perenne ssp. multiflorum, and characterize the underlying ALS-inhibitor resistance mechanism(s). Based on LD50 values, the MR1-A, MR1-P, and MR2 subpopulations were 38-, 29-, 8-fold and 36-, 64-, and 3-fold less sensitive to imazamox and mesosulfuron, respectively, relative to the susceptible (Sus) population. Only MR1-P and MR2 plants were cross-resistant to rimsulfuron, whereas both MR1 subpopulations were cross-resistant to imazethapyr. Pinoxaden (ACCase inhibitor [phenylpyrazoline 'DEN']) only controlled MR2 and Sus plants at the labeled field rate. However, all plants were effectively controlled (>99%) with the labeled field rate of glufosinate. Based on I50 values, MR1-A, MR-P, and MR2 plants were 712-, 1,104-, and 3-fold and 10-, 18-, and 5-fold less responsive to mesosulfuron and imazamox, respectively, than the Sus plants. Sequence alignment of the ALS gene of resistant plants revealed a missense single-nucleotide polymorphism resulting in a Trp-574-Leu substitution in MR1-A and MR1-P plants, heterozygous in both, but not in the MR2 plants. An additional homozygous substitution, Asp-376-Glu, was identified in the MR1-A plants. Addition of malathion or piperonyl butoxide did not alter the efficacy of mesosulfuron on MR2 plants. In addition, the presence of 2,4-D had no effect on the response of mesosulfuron on the MR2 and Sus. These results suggest an altered target site is the mechanism of resistance to ALS inhibitors in MR1-A and MR1-P plants, whereas a non–target site based resistance apparatus is present in the MR2 plants.

Several grass and broadleaf weed species around the world have evolved multiple-herbicide resistance at alarmingly increasing rates. Research on the biochemical and molecular resistance mechanisms of multiple-resistant weed populations indicate a prevalence of herbicide metabolism catalyzed by enzyme systems such as cytochrome P450 monooxygenases and glutathione S-transferases and, to a lesser extent, by glucosyl transferases. A symposium was conducted to gain an understanding of the current state of research on metabolic resistance mechanisms in weed species that pose major management problems around the world. These topics, as well as future directions of investigations that were identified in the symposium, are summarized herein. In addition, the latest information on selected topics such as the role of safeners in inducing crop tolerance to herbicides, selectivity to clomazone, glyphosate metabolism in crops and weeds, and bioactivation of natural molecules is reviewed.

Recently, several incidents of glyphosate failure on junglerice [Echinochloa colona (L.) Link] have been reported in the midsouthern United States, specifically in Mississippi and Tennessee. Research was conducted to measure the magnitude of glyphosate resistance and to determine the mechanism(s) of resistance to glyphosate in E. colona populations from Mississippi and Tennessee. ED50 (dose required to reduce plant growth by 50%) values for a resistant MSGR4 biotype, a resistant TNGR population, and a known susceptible MSGS population were 0.8, 1.62, and 0.23 kg ae ha−1 of glyphosate, respectively. The resistance index calculated from the these ED50 values indicated that the MSGR4 biotype and TNGR population were 4- and 7-fold, respectively, resistant to glyphosate relative to the MSGS population. The absorption patterns of [14C]glyphosate in the TNGR and MSGS populations were similar. However, the MSGS population translocated 13% more [14C]glyphosate out of the treated leaf compared with the TNGR population at 48 h after treatment. EPSPS gene sequence analyses of TNGR E. colona indicated no evidence of any point mutations, but several resistant biotypes, including MSGR4, possessed a single-nucleotide substitution of T for C at codon 106 position, resulting in a proline-to-serine substitution (CCA to TCA). Results from quantitative polymerase chain reaction analyses suggested that there was no amplification of the EPSPS gene in the resistant populations and biotypes. Thus, the mechanism of resistance in the MSGR population (and associated biotypes) is, in part, due to a target-site mutation at the 106 loci of the EPSPS gene, while reduced translocation of glyphosate was found to confer glyphosate resistance in the TNGR population.

Herbicide resistance, and in particular multiple-herbicide resistance, poses an ever-increasing threat to food security. A biotype of junglerice [Echinochloa colona (L.) Link] with resistance to four herbicides, imazamox, fenoxaprop-P-ethyl, quinclorac, and propanil, each representing a different mechanism of action, was identified in Sunflower County, MS. Dose responses were performed on the resistant biotype and a biotype sensitive to all four herbicides to determine the level of resistance. Application of a cytochrome P450 inhibitor, malathion, with the herbicides imazamox and quinclorac resulted in increased susceptibility in the resistant biotype. Differential gene expression analysis of resistant and sensitive plants revealed that 170 transcripts were upregulated in resistant plants relative to sensitive plants and 160 transcripts were upregulated in sensitive plants. In addition, 507 transcripts were only expressed in resistant plants and 562 only in sensitive plants. A subset of these transcripts were investigated further using quantitative PCR (qPCR) to compare gene expression in resistant plants with expression in additional sensitive biotypes. The qPCR analysis identified two transcripts, a kinase and a glutathione S-transferase that were significantly upregulated in resistant plants compared with the sensitive plants. A third transcript, encoding an F-box protein, was downregulated in the resistant plants relative to the sensitive plants. As no cytochrome P450s were differentially expressed between the resistant and sensitive plants, a single-nucleotide polymorphism analysis was performed, revealing several nonsynonymous point mutations of interest. These candidate genes will require further study to elucidate the resistance mechanisms present in the resistant biotype.

Field experiments were conducted in 1992 and 1993 to evaluate wirestem muhly control in no-till corn with application of glyphosate, nicosulfuron, and primisulfuron. Glyphosate was applied preplant at 1.1 kg ai/ha. Nicosulfuron and primisulfuron were applied at 0.018, 0.036, and 0.072 kg ai/ha and 0.020, 0.040, and 0.080 kg ai/ha, respectively, at four postemergence timings that included a split application. Similar experiments were conducted with wirestem muhly grown from rhizomes and seed in the greenhouse. Glyphosate was the most effective herbicide in the greenhouse, providing at least 96% control. However, preplant application of glyphosate in the field was ineffective in controlling wirestem muhly. On average, nicosulfuron and primisulfuron never exceeded 72% control of wirestem muhly in the greenhouse or in the field. Nicosulfuron was generally more effective than primisulfuron. Control with split application timings was more uniform over a 12-wk period than single applications and late postemergence applications were often too slow acting to affect wirestem muhly growth. Although neither nicosulfuron nor primisulfuron controls wirestem muhly, both can provide suppression of this weed where other alternatives do not exist.

Use of glyphosate in controlling Orobanche aegyptiaca (broomrape), a parasitic weed on dicotyledonous crops, was examined by determining glyphosate dose response and 14C-labeled glyphosate absorption, translocation, and metabolism patterns in Vicia sativa (common vetch) that is tolerant of low levels of glyphosate and Brassica napus (oilseed rape) that has been genetically engineered to be glyphosate resistant. Glyphosate provided excellent suppression of O. aegyptiaca growth in both V. sativa and B. napus. Absorption and translocation of 14C-glyphosate was similar between parasitized and nonparasitized V. sativa plants. 14C-Glyphosate was metabolized up to 32% in V. sativa, which could account for some of the tolerance of V. sativa to glyphosate. Approximately 27% of translocated 14C-glyphosate accumulated in O. aegyptiaca attachments on V. sativa. Absorption and translocation patterns of 14C-glyphosate were similar between parasitized and nonparasitized B. napus plants. Nearly one-third (31%) of the translocated radioactivity was found in O. aegyptiaca attachments on B. napus. No metabolism of 14C-glyphosate was detected in B. napus.

Greenhouse and field experiments were conducted to evaluate the effectiveness of nicosulfuron and primisulfuron with different adjuvants on wirestem muhly control. The adjuvants evaluated with the two herbicides included a nonionic surfactant, crop-oil concentrate, crop-oil concentrate plus urea-ammonium nitrate, methylated vegetable-oil concentrate, and organosilicone methylated vegetable-oil concentrate. In the greenhouse, nicosulfuron and primisulfuron performance was similar, although small differences occurred between adjuvants and herbicides. In the field, changing adjuvant affected nicosulfuron performance more than primisulfuron and in general, greater control was achieved with nicosulfuron than with primisulfuron. Among adjuvants, methylated vegetable-oil concentrate provided greater wirestem muhly control with nicosulfuron and sometimes primisulfuron compared to the others, while the nonionic surfactant was the least effective with both herbicides. Regardless of adjuvant, none of the field-applied treatments controlled wirestem muhly much beyond the 12 wk-evaluation period.

The influence of environmental factors on germination and emergence of horseweed was examined in growth chamber experiments. Germination was highest (61%) under 24/20 C day/night temperature under light. Horseweed seed germination was observed under both light (13 h photoperiod) and complete darkness (24 h), but germination under continuous darkness was only 0 to 15% compared with 0 to 61% under light. All other experiments were conducted under 24/20 C and 13-h light conditions. Germination was 19 to 36% over a pH range from 4 to 10, with a trend toward higher germination under neutral-to-alkaline conditions. Horseweed germination was > 20% at < 40 mM NaCl concentration and lowest (4%) at 160 mM NaCl. These data suggest that even at high soil salinity conditions, horseweed can germinate. Germination of horseweed decreased from 25% to 2% as osmotic potential increased from 0 (distilled water) to −0.8 MPa, indicating that germination can still occur under moderate water stress conditions. Horseweed seedling emergence was at its maximum on the soil surface, and no seedlings emerged from seeds placed at a depth of 0.5 cm or higher.

BAY MKH 6562 [flucarbazone-sodium (proposed)], an acetolactate synthase (ALS)-inhibiting herbicide of the sulfonylaminocarbonyltriazolinone family, provides postemergence wild oat control in wheat. Whole-plant dose responses and in vitro ALS sensitivity assays were used to evaluate the magnitude and nature of cross-resistance to BAY MKH 6562 in a wild oat accession (AR1) with metabolism-based resistance to imazamethabenz, an ALS inhibitor of the imidazolinone family. An imazamethabenz-susceptible wild oat accession (AHS2), five BAY MKH 6562-resistant wild oat accessions, AN104, AN205, AN307, AN406, and ASB11, and wheat were also evaluated. AHS2 and AR1 dose responses to BAY MKH 6562 indicated a resistant/susceptible (R/S) herbicide dose required to cause 50% growth reduction (GR50) ratio of 200. Inhibition of ALS from the AHS2 and AR1 wild oat by BAY MKH 6562 was similar, with a concentration of herbicide required to cause 50% inhibition of enzymatic activity (I50) of 0.007 µmoles, indicating that cross-resistance was not due to an altered ALS enzyme. The GR50 for BAY MKH 6562 for the AN104, AN205, AN307, AN406, and ASB11 wild oat accessions was 0.23, 0.07, 0.23, 0.22, and 0.12 kg ai/ha, respectively, and the R/S ratio to the GR50 value for the AHS2 accession was 230, 70, 230, 220, and 120, respectively. Studies on ALS sensitivity to BAY MKH 6562 indicated that the I50 for the AN104, AN205, AN307, AN406, and ASB11 wild oat accessions was 5.2, 0.003, 0.008, 9.8, and 0.007 µmoles, respectively, and the R/S ratio to the I50 value for the AHS2 accession was 759, 0.5, 1, 1,444, and 1, respectively. Of the five wild oat accessions resistant to BAY MKH 6562, accessions AN104 and AN406 had high R/S I50 ratios indicative of an altered target site and accessions AN205, AN307, and AR1 had low R/S I50 ratios indicative of resistance based on metabolic degradation. Hard red spring wheat (2371) was 800-fold tolerant to BAY MKH 6562 and inhibition of ALS from wheat by BAY MKH 6562 was similar to that of ALS from the susceptible accession AHS2.

Two Italian ryegrass populations from Mississippi, Tribbett and Fratesi, were suspected to be tolerant to glyphosate. A third population from Mississippi, Elizabeth, known to be susceptible to glyphosate, was included for comparison. Plants were treated with the isopropylamine salt of glyphosate at 0, 0.11, 0.21, 0.42, 0.84, 1.68, 3.36, and 6.72 kg ae/ha. GR50 (herbicide dose required to cause a 50% reduction in plant growth) values for the Tribbett, Fratesi, and Elizabeth populations were 0.66, 0.66, and 0.22 kg/ha, respectively, indicating that the Tribbett and Fratesi populations were threefold more tolerant to glyphosate compared with the Elizabeth population. These three populations were also treated with diclofop at 0, 0.13, 0.25, 0.5, 0.75, 1, and 2 kg ai/ha. Diclofop GR50 values for the Tribbett, Fratesi, and Elizabeth populations were 0.25, 0.28, 0.21 kg/ha, respectively, indicating similar tolerance to diclofop in the three populations. Response of all three populations to clethodim rate (0, 0.02, 0.03, 0.05, 0.06, 0.08, 0.09, and 0.13 kg ai/ha) was measured. Clethodim GR50 values for the Tribbett, Fratesi, and Elizabeth populations at the small growth stages were 0.016, 0.023, 0.014 kg/ha, respectively, and at the large growth stage were 0.04, 0.034, 0.02 kg/ha, respectively.

Greenhouse and laboratory studies were conducted to confirm and quantify glyphosate resistance, quantify pyrithiobac resistance, and investigate interaction between flumiclorac and glyphosate mixtures on control of Palmer amaranth from Mississippi. The GR50 (herbicide dose required to cause a 50% reduction in plant growth) values for two glyphosate-resistant biotypes, C1B1 and T4B1, and a glyphosate-susceptible (GS) biotype were 1.52, 1.3, and 0.09 kg ae ha−1 glyphosate, respectively. This indicated that the C1B1 and T4B1 biotypes were 17- and 14-fold resistant to glyphosate, respectively, compared with the GS biotype. The C1B1 and T4B1 biotypes were also resistant to pyrithiobac, an acetolactate synthase (ALS) inhibitor, with GR50 values of 0.06 and 0.07 kg ai ha−1, respectively. This indicated that the C1B1 and T4B1 biotypes were 7- and 8-fold, respectively, more resistant to pyrithiobac compared with the GS biotype, which had a GR50 value of 0.009 kg ha−1. Flumiclorac was antagonistic to glyphosate by reducing glyphosate translocation. The C1B1 and T4B1 absorbed less glyphosate 48 h after treatment (HAT) compared with the GS biotype. The majority of the translocated glyphosate accumulated in the shoot above the treated leaf (that contains the apical meristem) in the GS biotype and in the shoot below the treated leaf in the resistant biotypes, C1B1 and T4B1, by 48 HAT. The C1B1 biotype accumulated negligible shikimate levels, whereas the T4B1 and GS biotypes recorded elevated levels of shikimate. Metabolism of glyphosate to aminomethylphosphonic acid was not detected in either of the resistant biotypes or the susceptible GS biotype. The above results confirm multiple resistance to glyphosate and pyrithiobac in Palmer amaranth biotypes from Mississippi and indicate that resistance to glyphosate is partly due to reduced absorption and translocation of glyphosate.

2,4-D, discovered independently in the United States and Europe in the mid-1940s, was one of the first synthetic herbicides to be used selectively for weed control (Cobb and Reade 2010). Since then, several herbicides belonging to different chemical classes and possessing diverse mechanisms of action have been synthesized and marketed globally. Herbicides have vastly contributed to increasing world food, fiber, fuel, and feed production in an efficient, economic, and environmentally sustainable manner. Before receiving regulatory approval, all herbicides (pesticides) undergo rigorous testing for their toxicological, residual, physicochemical, and biological properties. Additionally, herbicides are suitably formulated to reach their target site and maximize their efficacy on target weeds while being safe on crops.

Smallflower umbrella sedge is a problematic weed in direct-seeded rice in the midsouthern United States. It recently has evolved resistance to the acetolactate synthase (ALS) –inhibiting herbicide halosulfuron in Arkansas rice. Studies were conducted (1) to determine if the resistant biotype is cross resistant to other ALS-inhibiting herbicides, (2) to evaluate alternative herbicide control options, and (3) to determine the mechanism of resistance. Whole-plant bioassay revealed that halosulfuron-resistant plants were not controlled by bispyribac–sodium, imazamox, and penoxsulam at the labeled field rate of each herbicide. The level of resistance to these herbicides, based on the lethal dose needed to kill 50% of plants (LD50) was ≥ 15-fold compared to a susceptible biotype. Both biotypes were controlled >96% with bentazon and propanil and ≤ 23% with quinclorac, thiobencarb, and 2,4-D. Hence, effective control measures exist; albeit, the number of herbicide options appear limited. Based on in vitro ALS enzyme assays, altered target site is the mechanism of resistance to halosulfuron and imazamox. Massively parallel sequencing with the use of the Illumina HiSeq detected an amino acid substitution of Pro197-to-His in the resistant biotype that is consistent with ALS-inhibiting herbicide resistance in other weed species.

Transfer of herbicide resistance among closely related weed species is a topic of growing concern. A spiny amaranth × Palmer amaranth hybrid was confirmed resistant to several acetolactate synthase (ALS) inhibitors including imazethapyr, nicosulfuron, pyrithiobac, and trifloxysulfuron. Enzyme assays indicated that the ALS enzyme was insensitive to pyrithiobac and sequencing revealed the presence of a known resistance conferring point mutation, Trp574Leu. Alignment of the ALS gene for Palmer amaranth, spiny amaranth, and putative hybrids revealed the presence of Palmer amaranth ALS sequence in the hybrids rather than spiny amaranth ALS sequences. In addition, sequence upstream of the ALS in the hybrids matched Palmer amaranth and not spiny amaranth. The potential for transfer of ALS inhibitor resistance by hybridization has been demonstrated in the greenhouse and in field experiments. This is the first report of gene transfer for ALS inhibitor resistance documented to occur in the field without artificial/human intervention. These results highlight the need to control related species in both field and surrounding noncrop areas to avoid interspecific transfer of resistance genes.

Inhibitors of acetolactate synthase (ALS) are important herbicides for control of wild mustard, a common weed of the north central United States and Canada. Wild mustard that survived treatments with the ALS inhibitors cloransulam, imazethapyr, and thifensulfuron was sampled from a North Dakota soybean field in 1999. The mechanism of resistance and response of this wild mustard biotype to ALS-inhibiting herbicides was investigated. In vitro enzyme-inhibition experiments confirmed a resistance mechanism associated with the ALS enzyme; imazethapyr or imazamox at 1 × 10−4 M caused only 10 to 11% and 12 to 16% reductions in ALS activity, respectively. ALS from a susceptible wild mustard biotype was inhibited 50% (I50) with imazethapyr at 8 × 10−7 M or imazamox at 1.1 × 10−6 M. Whole-plant greenhouse treatments confirmed cross-resistance across ALS-inhibitor classes. Treatment with twice-normal field rates of thifensulfuron, ethametsulfuron, triflusulfuron, imazamox, imazethapyr, flumetsulam, cloransulam, flucarbazone, and imazamethabenz reduced biomass of the susceptible biotype at least 96% 28 d after treatment. Biomass of the resistant biotype was reduced 49% by triflusulfuron and 35% by thifensulfuron, but was not reduced by other herbicides. DNA sequence analysis of ALS genes from resistant and susceptible biotypes revealed a point mutation inferring a Trp-to-Leu amino acid substitution in ALS of the resistant biotype. This mutation, corresponding to position 574 of the Arabidopsis ALS amino acid sequence, is known to confer cross-resistance to ALS-inhibiting herbicides and is the probable cause of resistance in the wild mustard biotype. Phylogenetic analysis of wild mustard and canola ALS sequences confirmed that the Trp574 mutation arose within wild mustard and was not derived via introgression from imidazolinone-resistant canola. The results of this research indicate a naturally occurring target-site point mutation responsible for conferring cross-resistance to ALS-inhibiting herbicides in this wild mustard biotype.

A threefold glyphosate tolerance was identified in two Italian ryegrass populations, T1 and T2, from Mississippi. Laboratory experiments were conducted to characterize the mechanism of glyphosate tolerance in these populations. The T1 population absorbed less 14C-glyphosate (43% of applied) compared to the susceptible (S) population (59% of applied) at 48 h after treatment (HAT). The T2 population absorbed 14C-glyphosate at levels (56% of applied at 48 HAT) that were similar to both T1 and S populations, but tended to be more comparable to the S population. The amount of 14C-glyphosate that remained in the treated leaf was significantly higher in both T1 (67% of absorbed) and T2 (65% of absorbed) populations compared to the S population (45% of absorbed) at 48 HAT. The amount of 14C-glyphosate that moved out of treated leaf to shoot and root was lower in both T1 (25% of absorbed in shoot and 9% of absorbed in root) and T2 (25% of absorbed in shoot and 11% of absorbed in root) populations compared to the S population (40% of absorbed in shoot and 16% of absorbed in root) at 48 HAT. There were no differences in epicuticular wax mass among the three populations. Treating a single leaf with glyphosate solution at the field use rate (0.84 kg ae ha−1) as 10 1-µl droplets killed the S plant but not the T1 and T2 plants (33 and 55% shoot fresh-weight reduction, respectively). Shikimic acid accumulated rapidly at higher levels in glyphosate-treated leaf segments of the S population compared to the T1 population up to 100 µM glyphosate. However, above 500 µM glyphosate, the levels of shikimate were similar in both the S and T1 populations. Furthermore, shikimic acid content was three- to sixfold more in whole plants of the S population treated with 0.22 kg ae ha−1 glyphosate compared to the T1 and T2 populations. No degradation of glyphosate to aminomethylphosphonic acid was detected among the tolerant and susceptible populations. These results indicate that tolerance to glyphosate in the T1 population is partly due to reduced absorption and translocation of glyphosate and in the T2 population it is partly due to reduced translocation of glyphosate.

Auxin-type herbicides such as 2,4-D and dicamba are commonly used to control kochia in small grain production areas, but poor kochia control with these herbicides has been reported. Several auxinic herbicide-resistant kochia inbreds were evaluated for their response to 2,4-D or dicamba and to alternative herbicide treatments. Values of the dose of the herbicide causing 50% visible injury to test plants (I50) from week 1 to week 4 after treatment with 2,4-D were unchanged for six of the seven 2,4-D–resistant inbreds, indicating that these plants may recover to produce seeds. In contrast, the corresponding I50 values for dicamba decreased for five of the six dicamba-resistant inbreds, indicating that kochia was not recovering from the treatment. Postemergence treatments with atrazine, carfentrazone, fluroxypyr, bromoxynil plus MCPA, nicosulfuron plus dicamba, and nicosulfuron plus dicamba plus atrazine, all provided adequate to excellent control of resistant kochia inbreds. Alternative chemical control options are available for managing auxinic herbicide-resistance in kochia.

Overuse of acetolactate synthase (ALS)–inhibiting herbicides in rice has led to the evolution of halosulfuron-resistant rice flatsedge in Arkansas and Mississippi. Resistant accessions were cross-resistant to labeled field rates of ALS-inhibiting herbicides from four different families, in comparison to a susceptible (SUS) biotype. Resistance index of Arkansas and Mississippi accessions based on an R/S ratio of the lethal dose required for 50% plant mortality (LD50) to bispyribac-sodium, halosulfuron, imazamox, and penoxsulam was ≥ 21-fold. Control of Arkansas, Mississippi, and SUS accessions with labeled field rates of 2,4-D, bentazon, and propanil was ≥ 93%. An enzyme assay revealed that an R/S ratio for 50% inhibition (I50) of ALS for halosulfuron was 2,600 and 200 in Arkansas and Mississippi, respectively. Malathion studies did not reveal enhanced herbicide metabolism in resistant plants. The ALS enzyme assay and cross-resistance studies point toward altered a target site as the potential mechanism of resistance. Trp574–Leu amino acid substitution within the ALS gene was found in both Arkansas and Mississippi rice flatsedge accessions using the Illumina HiSeq platform, which corresponds to the mechanism of resistance found in many weed species. Field-rate applications of 2,4-D, bentazon, and propanil can be used to control these ALS-resistant rice flatsedge accessions.