Tall fescue is susceptible to injury from many acetolactate synthase (ALS) inhibitors used for broadleaf weed control in turfgrass. Florasulam is an ALS inhibitor that selectively controls broadleaf weeds in tall fescue, but the mechanisms for selectivity are not well understood. The objective of this research was to evaluate the physiological basis of tall fescue tolerance to florasulam. In greenhouse experiments, florasulam rates required to injure tall fescue 20% (I20) and white clover 80% (I80) measured 320 and 65 g ai ha–1, respectively. The I20 and I80 values of another ALS inhibitor, flucarbazone, on these species measured 33 and 275 g ai ha–1, respectively. In laboratory experiments, the time required to reach 50% foliar uptake for 14C-florasulam and 14C-flucarbazone measured 23 and 62 h for white clover, respectively, and >72 h for both herbicides in tall fescue. The half-lives of florasulam and flucarbazone in tall fescue were 15 and 40 h, respectively, whereas the half-life in white clover was >72 h for both herbicides. The concentrations of florasulam and flucarbazone required to inhibit ALS enzymes 50% in excised leaves of tall fescue measured >1,000 and 32 μM, respectively. The selectivity of florasulam for white clover control in tall fescue is associated with differential levels of absorption and metabolism between species. Tall fescue has faster metabolism and less ALS enzyme inhibition from florasulam as compared to a more injurious ALS inhibitor, flucarbazone, which contributes to the differential tolerance levels between these herbicides.

American sloughgrass is a troublesome grass weed in winter wheat fields after rice in China. Mesosulfuron-methyl failed to control American sloughgrass in Danyang County in 2012. The purpose of this research was to determine the resistance level to mesosulfuron and other herbicides in American sloughgrass and to identify the molecular basis of resistance. Dose–response experiments indicated that this population was moderately resistant to mesosulfuron-methyl (7.6-fold) and pyroxsulam (6.0-fold), highly resistant to flucarbazone-sodium (20.3-fold), fenoxaprop-p-ethyl (565.0-fold), clodinafop-proargyl (19.5-fold), and pinoxaden (45.9-fold), and susceptible to isoproturon. Part of the acetolactate sythase (ALS) gene was cloned and sequenced to confirm the molecular mechanism of resistance to ALS-inhibiting herbicides. A Pro197Ser substitution was identified. This substitution is likely the molecular mechanism of resistance to mesosulfuron-methyl in the Danyang population in which it is cross-resistant to flucarbazone-sodium and pyroxsulam. This study established the first report of mesosulfuron-methyl resistance likely caused by a Pro197 substitution in American sloughgrass and a potential herbicide to control this resistant weed.

Many herbicides that control broadleaf weeds in wheat can antagonize grass herbicide efficacy, resulting in less grain yield due to competition. Also, the broadleaf herbicide carfentrazone-ethyl can injure wheat, leading to less grain yield because of physiological response. Experiments were conducted to evaluate carfentrazone-ethyl antagonism of fenoxaprop-ethyl, tralkoxydim, clodinafop-propargyl, imazamethabenz, and flucarbazone-sodium and injury to wheat with tank mixes of carfentrazone-ethyl plus each grass herbicide or thifensulfuron, tribenuron, metsulfuron, or imazamox. Carfentrazone-ethyl did not adversely affect control of wild oat or yellow foxtail by grass herbicides in wheat. Carfentrazone-ethyl alone caused 21% wheat injury 3 d after treatment. Adding flucarbazone-sodium to carfentrazone-ethyl resulted in the least wheat injury among treatments that included carfentrazone-ethyl. Fenoxaprop-P-ethyl or clodinafop-propargyl with carfentrazone-ethyl also resulted in less wheat injury compared with carfentrazone-ethyl alone, which was attributed to formulation safeners. Sulfonylurea herbicides provided safening of carfentrazone-ethyl similar to flucarbazone-sodium, while imidazolinones did not alleviate injury. Tralkoxydim plus carfentrazone-ethyl gave 28% wheat injury compared with 21% from carfentrazone-ethyl alone. Wheat injury was no longer visible by 20 d after treatment, and wheat yield was not affected by carfentrazone-ethyl injury when wild oat and yellow foxtail were present or controlled with herbicide.

Flucarbazone-sodium, a new herbicide, exhibits high bioactivity at low concentrations. To elucidate potential carryover and crop injury, the behavior of flucarbazone in six Western Canadian soils was studied in the laboratory. A sensitive bioassay was developed for the detection of flucarbazone. Of five crops tested, oriental mustard showed the highest degree of root and shoot inhibition from the presence of flucarbazone in soil. Flucarbazone concentrations as low as 1 μg kg−1 were detected by the mustard root inhibition method. This bioassay was used to examine phytotoxicity and persistence of flucarbazone. Phytotoxicity was related to soil organic carbon content. Concentrations corresponding to 50% inhibition (I 50 values) were estimated after fitting the data to a log-logistic model. I 50 estimates ranged from 6.0 to 27.5 μg kg−1 for soils containing 1.1 to 4.3% organic carbon, respectively, and were correlated (R = 0.979) with percent organic carbon in the investigated soils. Persistence of flucarbazone was examined in soils incubated at 25 C and moisture content of 85% field capacity (FC). Flucarbazone dissipation followed first-order kinetics in one soil, but a two-compartment model provided the best fit for dissipation in the other soils. Half-lives (t0.5), calculated from dissipation curves in each soil, ranged from 6 to 110 d. Half-lives were correlated (R = 0.776) with soil organic carbon. Flucarbazone dissipation was more rapid in soils containing less organic carbon. Flucarbazone was more persistent in drier soil; t0.5 was 11 d in soil at 85% FC and was 25 d in soil at 50% FC. Soil characteristics and environmental conditions will affect the degree of plant injury to sensitive crops the year after flucarbazone application.