The recent decline in pollinator abundance is a cause of concern for sustaining global food production. Several common weeds of managed turfgrass systems attract honeybees and other wild pollinators. As turfgrass often requires treatment with insecticides that harm bees, best practices are needed to prevent bees from visiting weed-infested turf areas that will be treated for insect pests. Weed control tactics can protect pollinator exposure to insecticides by reducing the floral resources afforded to bees from turfgrass weeds. Three field studies were conducted in 2021 and 2022 to evaluate the effect of various herbicides and herbicide formulation constituents on pollinator foraging and white clover floral morphology in managed tall fescue turfgrass. Treatments included a nontreated control; MCPP; 2,4-D; dicamba; Trimec Classic™ (2,4-D, MCPP, dicamba); Speedzone™ (carfentrazone, 2,4-D, MCPP, dicamba); and an herbicide-formulation constituent (inert ingredients of Speedzone™). All response variables were evaluated for 8 d, starting from one day before treatment and ending 6 d after treatment (DAT). The herbicide formulation constituent did not alter white clover flower density, floral discoloration, floral quality, or insect visitation compared to nontreated plots. Herbicides reduced flower density and floral quality to the same extent, but MCPP discolored white clover floral tissue 16% per day and less than all other herbicides except dicamba. Floral quality completely declined in approximately 5 d following any herbicide treatment. Bee visitation to white clover–infested turf increased by 3 bees min–1 for every 100 white clover blooms m–2. Honeybees and other insects vacated herbicide-treated areas in less than 2 d, despite minimal effects on floral quality and density at that time. The data suggest that practitioners could apply insecticides 2 d after auxin herbicide treatment and avoid harm to pollinators, but additional work is needed to directly measure pollinator exposure following such treatments.

Herbicide management information is lacking for recently developed turf-type bahiagrass germplasm. The objective of this study was to evaluate the herbicide tolerance of nine experimental bahiagrass genotypes compared to the industry standard ‘Argentine’. The experimental entries included Argentine and ‘Wilmington’ mutants, and wild-type breeding lines. Plants were grown under greenhouse conditions, and 12 herbicides were applied at 1× and 2× labeled rates. Bentazon, bromoxynil, carfentrazone + 2,4-D + MCPP + dicamba, and carfentrazone were classified as safe. Fluroxypyr, halosulfuron, and triclopyr + clopyralid reduced growth >50% when applied at twice the label rate. Fenoxaprop, sulfentrazone + imazethapyr, and thiencarbazone + iodosulfuron + dicamba reduced growth and caused turfgrass injury above an acceptable threshold (≥20%). In general, the Argentine mutants showed greater herbicide injury compared to the Wilmington mutants. However, metsulfuron exceeded the acceptable injury threshold and stopped growth in all the genotypes, Argentine and genotype WT6 were the least injured by this herbicide. The experimental genotype WT6 consistently showed the greatest herbicide tolerance. Except for one genotype (WT4), the experimental genotypes responded similarly or better than Argentine to the tested herbicides, except for metsulfuron.

The herbicide 2,4-D is used in a variety of cropping systems, especially in grasses because it is a selective postemergence broadleaf herbicide. However, the most common formulation (2,4-D dimethylamine) is antagonized when mixed in hard water. The objective of this research was to determine which formulations of 2,4-D or premixes of various formulations of synthetic auxin herbicides are subject to hard water antagonism. Formulations surveyed for hard water antagonism in the first experiment included 2,4-D dimethylamine, 2,4-D diethanolamine, 2,4-D monomethylamine, 2,4-D isopropylamine salt, 2,4-D choline salt, 2,4-D isooctyl ester, and 2,4-D ethylhexyl ester. Synthetic auxin formulation types in the second experiment included water-soluble, emulsifiable concentrates and emulsion-in-water. All formulations were mixed with both soft and hard water (600 mg CaCO3 L−1) and applied to dandelions to determine whether antagonism occurred in hard water. Water-soluble (amine and choline) 2,4-D formulations were antagonized by hard water, but water-insoluble (ester) 2,4-D formulations were not antagonized. Similar results were found by formulation type with water-soluble synthetic auxin premixes antagonized but emulsifiable concentrates not antagonized. Furthermore, water-soluble salt formulations were not antagonized when formulated in premixes with other synthetic auxin herbicides as an emulsion-in-water. This research demonstrates that all 2,4-D water-soluble formulations and water-soluble premixes with phenoxycarboxylic acid herbicides are subject to hard water antagonism. Formulations of 2,4-D containing emulsifying agents protect against antagonism by the water-insoluble nature of ingredients in their formulation.

The incidence of auxinic herbicide resistance in plants has increased worldwide. Auxinic herbicides were the first selective organic herbicides developed and have been used in agriculture for over 50 yr, primarily for the selective control of broadleaf weeds in cereal crops. However, the mode of action of auxinic herbicides and the molecular basis of auxinic herbicide resistance remain unknown, although an auxin-binding protein (ABP) is proposed to be the primary target site. Using auxinic herbicide-resistant (R) and -susceptible (S) biotypes of wild mustard as a model system, we have extensively studied the mode of action of auxinic herbicides and the resistance mechanisms at the physiological, biochemical, and molecular genetic levels. There are no differences in uptake, transport, and metabolism of auxinic herbicides between the R and S biotypes. Based on these results, as well as the studies on the role of auxin-enhanced ethylene biosynthesis and calcium in mediating the auxinic herbicide resistance, we hypothesize that resistance of the R biotype to auxinic herbicides is due to an altered target site, possibly an auxin receptor. We have identified and characterized a small ABP gene family as well as their cDNAs from both R and S of wild mustard. Amino acid changes were found in the ABP of the R biotype. Functional and mutational analyses of these genes are underway to determine the role of ABP in mediating auxinic herbicide resistance. In this review, we focus on the mode of action of auxinic herbicides and the molecular basis of auxinic herbicide resistance in wild mustard.

The role of calcium in mediating resistance to several auxinic herbicides (i.e., 2,4-dichlorophenoxyacetic acid, [4-chloro-2-methylphenoxy] acetic acid, (±)-2-(4-chloro-2-methylphenoxy) propanoic acid [mecoprop], 3,6-dichloro-2-methoxy-benzoic acid [dicamba], or 4-amino-3, 5,6-trichloro-2-pyridinecarboxylic acid [picloram]) was investigated by modulating calcium dynamics of a susceptible (S) and resistant (R) biotype of wild mustard. The inhibitory effects of the auxinic herbicides on root length of the S seedlings were significantly reduced upon pretreatment with calcium in the presence of the calcium ionophore A23187. Conversely, the addition of verapamil, a calcium channel blocker, to the R seedlings increased their sensitivity to the auxinic herbicides. Valinomycin, a potassium channel ionophore, did not ameliorate the effect of the auxinic herbicides on both biotypes of wild mustard, thus indicating that the observed effects were specific for calcium. These results demonstrate that calcium plays a crucial role in the resistance of wild mustard to auxinic herbicides at the level of intact seedlings, thereby supporting our previous results using intact protoplasts.

Studies examined the effect of herbicides on the quality and root strength of winter-installed tall fescue and hybrid bermudagrass sod. Sod was installed in February and treated approximately 30 to 45 d after installation with a variety of preemergence (PRE) and postemergence (POST) herbicides. Tall fescue quality was not affected by any herbicide treatment in 2000 or 2001. Root strength reduction occurred only in 2001 by dithiopyr applied PRE at 2.5 kg ai/ha, which is 4.5 times the maximum use rate. No other herbicides decreased tall fescue root strength in either year. Bermudagrass quality was decreased by triclopyr plus clopyralid applied POST, which resulted in 22 and 6% injury 42 d after initial treatment (DAIT) in 2000 and 2001, respectively. However, POST herbicides did not affect bermudagrass root strength in either year. PRE herbicide treatments did not reduce root development in bermudagrass in 2000. However, dithiopyr applied at 0.84 and 2.5 kg/ha reduced bermudagrass rooting by 59 and 70%, 60 DAIT, in 2001. Pendimethalin reduced root development of bermudagrass by 62% when applied at 10.2 kg/ha, three times the maximum use rate, in 2001. However, by 120 DAIT, only dithiopyr applied at 2.5 kg/ha decreased bermudagrass root development.

Meadow knapweed is a fertile European hybrid between black and brown knapweed that has expanded its North American distribution to 27 of the United States and four provinces in Canada. Two experiments were conducted on meadow knapweed in northwestern Washington to determine (1) whether meadow knapweed is similarly sensitive to several herbicides commonly used to control related knapweeds, (2) if herbicide application timing plays a role in control of meadow knapweed, and (3) whether mowing before, after, or instead of herbicide treatment can aid in meadow knapweed control. In the first experiment, herbicides were applied to meadow knapweed at rosette or bolting stages of growth, and again with the same herbicides in the autumn. In the summer following treatment, clopyralid alone or with 2,4-D, dicamba + 2,4-D, and triclopyr ester + 2,4-D ester provided 81 to 100% meadow knapweed control; the only other treatment providing similar control was glyphosate + ammonium sulfate applied at bolting and in autumn in the 2004 to 2005 trial. In the second experiment, combinations of mowing and dicamba + 2,4-D were applied at rosette or early flowering stages of growth. In the 2002 to 2003 trial, control when dicamba + 2,4-D was used exceeded 90%, except when meadow knapweed was mowed at rosette and sprayed at early flowering (78% control). Mowing twice the previous year had only a slight effect on meadow knapweed (10% control). Grass biomass exceeded meadow knapweed biomass in all herbicide-treated plots. In the 2004 to 2005 trial, meadow knapweed control and grass biomass was maximized when plots were mowed at rosette and treated with dicamba + 2,4-D at early flowering or when treated twice with these herbicides; these were the only treatments where grass biomass exceeded meadow knapweed biomass.

Path rush can become problematic on golf course fairways, especially on roughs where continuous golf cart or maintenance equipment traffic occurs. Research trials conducted in 2003 and 2004 compared the efficacy of 2,4-D and mixtures containing 2,4-D in single or sequential applications to herbicides without 2,4-D for path rush control in bermudagrass roughs. Sequential applications of 1.1 kg ae/ha 2,4-D or 0.8 + 0.2 + 0.1 kg ae/ha 2,4-D + MCPP + dicamba provided 95% path rush control with no injury to bermudagrass, 15 wk after initial treatment (WAIT). Single applications of 1.1 + 0.3 + 0.1 kg/ha 2,4-D + MCPP + dicamba or 1.1 kg/ha 2,4-D provided at least 81% path rush control, 15 WAIT. Treatments without 2,4-D did not provide acceptable levels of control (34% or less, 15 WAIT). 2,4-D applied alone or in preformulated mixtures provided excellent path rush control compared to treatments without 2,4-D. Sequential applications of these treatments provided greater path rush control than single applications. However, only the sequential application of 0.8 + 0.2 + 0.1 kg/ha 2,4-D + MCPP + dicamba provided greater path rush control than the single application. Results from these studies suggest that 2,4-D is a key herbicide for path rush control.