False-green kyllinga is a problematic C4 perennial Cyperaceae species. Previous research examined herbicide efficacy but has not integrated nonchemical practices with herbicides. Replicate field experiments were conducted to evaluate late-summer postemergence applications of herbicides in combination with turf-type tall fescue interseeding for false-green kyllinga control. Seven herbicide treatments and a nontreated control formed a complete factorial, with tall fescue interseeding or no seeding (eight-by-two factorial). Six herbicide treatments consisted of single postemergence applications of halosulfuron-methyl (70 g ha–1), imazosulfuron (420 g ha–1), and sulfentrazone + carfentrazone (280 + 30 g ha–1) applied 4 wk before tall fescue interseeding (WBS) and the day of interseeding. Glyphosate (220 g ae ha–1) applied the day of interseeding was the seventh herbicide treatment. Tall fescue was interseeded in September, and false-green kyllinga control was evaluated the following summer. In combination with tall fescue interseeding, imazosulfuron and halosulfuron applied 4 WBS as well as glyphosate applied the day of interseeding controlled false-green kyllinga better than all other treatments. In July, imazosulfuron and halosulfuron treatments applied 4 WBS and combined with interseeding had 1% to 6% false-green kyllinga cover, respectively, compared to 28% and 62% cover, respectively, without interseeding. Interseeding alone controlled false-green kyllinga <50%. Imazosulfuron, halosulfuron, and sulfentrazone + carfentrazone applied the day of seeding severely injured emerging tall fescue seedlings and reduced turfgrass quality the following spring. Applying imazosulfuron or halosulfuron in late summer and interseeding turf-type tall fescue 4 wk later or applying glyphosate the day of seeding are effective strategies for postemergence false-green kyllinga control. Integrating herbicides and the cultural practice of tall fescue interseeding provided more false-green kyllinga control than either practice alone.

Acetolactate synthase (ALS) inhibitors provide postemergence control of green kyllinga (Kyllinga brevifolia Rottb.) in turfgrass and other cropping systems. A suspected resistant (R) biotype of K. brevifolia was collected from a golf course and evaluated for resistance to ALS inhibitors. In greenhouse experiments, the sulfosulfuron rates required to cause 50% shoot biomass reduction from the nontreated at 4 wk after treatment (WAT) were 10 and 792 g ai ha−1 for the susceptible (S) and R biotypes, respectively. The rates required to cause 50% injury at 4 WAT were 189 and >3,360 g ai ha−1, respectively. In other experiments, shoot mass of the R biotype was not reduced by imazaquin, trifloxysulfuron-sodium, pyrimisulfan, thiencarbazone + foramsulfuron + halosulfuron, florasulam + halauxifen-methyl, and bentazon compared with the nontreated, while sulfentrazone reduced biomass similarly for both R and S biotypes. Gene sequencing of the R biotype revealed a mutation at Asp-376-Glu that has previously conferred resistance to five families of ALS inhibitors. This is the first report of ALS-inhibitor resistance in K. brevifolia.

We conducted research to evaluate various herbicides for POST false-green kyllinga control in cool-season turfgrass (primarily creeping bentgrass). In a preliminary evaluation, single and sequential applications of halosulfuron-methyl (70 g ai ha−1), mesotrione (175 g ai ha−1), and sulfentrazone (140 g ai ha−1), as well as a single application of imazosulfuron (740 g ai ha−1), were evaluated in New Jersey. Imazosulfuron and sequential applications of halosulfuron-methyl controlled false-green kyllinga >93% at 9 and 18 wk after initial treatment (WAIT). Sulfentrazone and mesotrione controlled false-green kyllinga <50%. Additional experiments were conducted to evaluate single and sequential applications of halosulfuron-methyl (70 g ha−1), imazosulfuron (420 and 740 g ha−1), and sulfentrazone (140 g ha−1) in New Jersey and Indiana at two locations in each state. At 12 WAIT, imazosulfuron generally controlled false-green kyllinga more effectively than other treatments at all locations. Sequential applications of imazosulfuron controlled false-green kyllinga 100% at 12 WAIT. Halosulfuron-methyl was less effective in Indiana than in New Jersey. Sulfentrazone controlled false-green kyllinga <40% at 12 WAIT. This research demonstrates that imazosulfuron is more effective than halosulfuron-methyl and sulfentrazone for POST false-green kyllinga control in cool-season turf.

Egyptian broomrape (Phelipanche aegyptiaca Pers.) is a root-parasitic weed that severely damages many crops worldwide, including tomato (Solanum lycopersicum L.). In Israel, the management protocol used for P. aegyptiaca in open-field tomato includes PPI sulfosulfuron at 37.5 g ai ha−1 to the top 10-cm soil layer. The objective of this study was to investigate the co-effect of sulfosulfuron application timing and variable degradation rate in soil on the control efficacy of P. aegyptiaca in tomato. Degradation of sulfosulfuron (80ng g−1 soil) at a temperature of 15C, measured in soil samples from three farms using liquid chromatography–tandem mass spectrometry, followed a first-order kinetics with variable degradation rate constant among sites (0.008 to 0.012 d−1). Incubation at 25 C increased sulfosulfuron degradation rate constant by a factor of 2 to 2.7 in soils from the different sites, with a similar degradation rate order among soils. A higher degradation rate in the soil resulted in a shorter period of residual activity, measured using a sorghum [Sorghum bicolor (L.) Moench.] bioassay. Phelipanche aegyptiaca management in open-field tomatoes was investigated in five independent field experiments. Sulfosulfuron soil concentration throughout the growing season (following preplant incorporation of 37.5 g ha−1) was calculated from laboratory-measured degradation rates, which were corrected to represent the effect of recorded temperatures at each field. At the end of the tomato growing season, control efficacy of P. aegyptiaca varied among experiments (70.4% to 100%) and positively correlated with predicted sulfosulfuron concentration at the critical period for seedling control (R2=0.67). The current study confirms that sulfosulfuron is degraded in soil to nonphytotoxic metabolites and that rapid degradation rates would result in reduced injury to P. aegyptiaca seedling and, consequently, lower control efficacy.

Greenhouse studies were conducted to investigate the absorption, translocation, and metabolism of foliar-applied [14C]halosulfuron-methyl in cucumber, summer squash, pitted morningglory, and velvetleaf. Cucumber and summer squash were treated at the 4-leaf stage, whereas velvetleaf and pitted morningglory were treated at 10 cm. All plants were collected at 4, 24, 48, and 72 h after treatment (HAT) for absorption and translocation studies and an additional 96-HAT interval was included in the metabolism study. Absorption did not exceed 45% in summer squash, whereas it plateaued around 60% in velvetleaf and cucumber and reached 80% in pitted morningglory 72 HAT. None of the four species translocated more than 23% of absorbed halosulfuron out of the treated leaf. Translocation in cucumber and summer squash was predominantly basipetal, while acropetal movement prevailed in velvetleaf. No significant direction of movement was observed for pitted morningglory. Negligible translocation occurred toward the roots, regardless of plant species. Of the total amount of [14C]halosulfuron-methyl absorbed into the plants at 96 HAT, more than 80% remained in the form of the parent compound in velvetleaf, summer squash, and pitted morningglory, whereas less than 20% was detected in cucumber. Rapid and high herbicide metabolism may explain cucumber tolerance to halosulfuron-methyl, while lack of metabolism contributes to summer squash and velvetleaf susceptibility. Pitted morningglory tolerance may be due to limited translocation associated with some level of metabolism, but further research would be needed to investigate other potential causes.

In 1993, a wild mustard population growing in a canola crop near Wetaskiwin, AB was poorly controlled by ethametsulfuron after only one previous use of the herbicide. Controlled environment experiments were conducted to compare the response of this suspected resistant population (R) with that of a known susceptible population (S) collected near Vegreville, AB to increasing rates of ethametsulfuron, metsulfuron, chlorsulfuron, thifensulfuron, HOE 075032, imazamethabenz, imazethapyr, metribuzin, and 2,4-D. The R wild mustard population was highly resistant to ethametsulfuron, slightly resistant to low rates of metsulfuron but not resistant to any of the other herbicides tested. This suggests that the mechanism of resistance may differ from that reported for other sulfonylurea and imidazolinone herbicides. Since resistance was documented after only 2 yr of ethametsulfuron use, the initial frequency of resistance to this herbicide in wild mustard populations may be very high. Dry weight of untreated plants did not differ significantly between the S and R populations suggesting little or no differences in competitiveness between them.

Microsomes (100,000 g pellet containing mixed membrane fractions but primarily endoplasmic reticulum) were isolated from shoots of corn, shattercane, and woolly cupgrass grown from naphthalic anhydride treated or untreated seed to determine if metabolism of bentazon, nicosulfuron, and primisulfuron could be demonstrated in the preparations. Corn is tolerant of all three herbicides, shattercane is tolerant of bentazon, and woolly cupgrass is tolerant of bentazon and primisulfuron. Naphthalic anhydride treatment was required for detectable bentazon, nicosulfuron, and primisulfuron hydroxylation in corn microsomes and for bentazon hydroxylation in woolly cupgrass microsomes. Bentazon hydroxylation was low, but detectable, in microsomes from shattercane shoots without naphthalic anhydride treatment. Naphthalic anhydride-treated corn microsomes hydroxylated 292, 120, and 52 pmol mg−1 protein min−1 of bentazon, nicosulfuron, and primisulfuron, respectively. Primisulfuron (19 pmol mg−1 protein min−1), but not nicosulfuron, was hydroxylated in woolly cupgrass microsomes. Neither nicosulfuron nor primisulfuron was hydroxylated in shattercane microsomes. Bentazon and primisulfuron inhibited nicosulfuron hydroxylation in corn microsomes. Bentazon, but not nicosulfuron, also inhibited primisulfuron hydroxylation in the corn microsomes. This indicates that the three herbicides can interact at the same cytochrome P-450(s) in corn. Primisulfuron hydroxylation was not inhibited by either bentazon or nicosulfuron in woolly cupgrass microsomes. This suggests that the cytochrome P-450(s) for primisulfuron hydroxylation are different between corn and woolly cupgrass. Also, bentazon hydroxylation in corn and shattercane microsomes was inhibited by the cytochrome P-450 inhibitor tetcyclasis, while that in woolly cupgrass was not. Again, this suggests a difference in the cytochrome P-450(s) responsible for bentazon metabolism among the species. Although absolute conclusions comparing in vitro microsomal activities to whole plant herbicide tolerance cannot be made because it is unknown whether the same cytochrome P-450(s) are studied in microsomes from naphthalic anhydride-treated tissue as are responsible for in vivo herbicide metabolism, there was a broad correlation between metabolism of a particular herbicide in microsomes of a species and the species' tolerance of that herbicide.

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.

The overall degradation of chlorimuron was very similar at −0.1 and −1.5 MPa and slightly less in air-dry soil. Degradation rates increased with increasing temperature. The primary 14C-labeled compounds observed in moist-soil extracts were desmethyl chlorimuron and saccharin, while the primary 14C-labeled compound observed in air-dry soil extracts was saccharin. Saccharin is formed quantitatively from ethyl 2-(aminosulfonyl)benzoate (phenylsulfonamide) during extraction and therefore represents phenylsulfonamide formed in the soil as a result of chemical hydrolysis of the sulfonylurea bridge. These degradation products suggest that chemical hydrolysis of the sulfonylurea bridge is the primary mode of degradation in air-dry soil, while microbial degradation and chemical hydrolysis both occur in moist soil. These laboratory results demonstrate that chlorimuron will degrade in air-dry soil at a temperature-dependent rate by chemical hydrolysis.

Greenhouse experiments were conducted to determine ‘Len’ hard red spring wheat response to triallate and chlorsulfuron applied separately and together. Chlorsulfuron at 12 or 23 g/ha plus preplant incorporated (PPI) triallate at 1120 g/ha antagonized triallate toxicity to wheat. Chlorsulfuron reduced triallate injury to wheat less when applied preemergence (PRE) after PPI triallate compared to both herbicides applied PPI. Soaking wheat seeds in 21 and 31 ppbw chlorsulfuron solutions for 24 h before placing into triallate-treated soil did not reduce triallate injury to wheat. Applying chlorsulfuron to triallate did not reduce triallate toxicity to wild oats.

Kansas and North Dakota kochia populations identified as chlorsulfuron resistant (R) contained 20 and 30% susceptible (S) plants, respectively. Biotypes that were chlorsulfuron R or S were selected from each field R or S collection and selfed through three generations in the greenhouse. Chlorsulfuron at 7.6 and 17.8 g ai/ha suppressed shoot biomass of the Kansas and North Dakota R biotypes by 50%, respectively, which was a 30- and 105-fold greater dose than that required to reduce the respective S biotypes growth 50%. The R and S kochia biotypes are diploid with 2N = 18 chromosomes. Chlorsulfuron resistance is inherited in kochia as a dominant trait controlled by a single nuclear gene. Thus, the resistance trait can be spread by seed and pollen.

Chlorsulfuron {2-chloro-N-[[(4-methoxy-6-methyl-1,3,5-triazin-2-yl)amino] carbonyl]-benzenesulfonamide} applied preemergence or postemergence as a soil drench retards the growth of four corn (Zea mays L.) genotypes in soil with 50% inhibition in each case at a rate of approximately 5 g ai/ha. R-25788 (N,N-diallyl-2,2-dichloroacetamide), applied at 1.0 kg ai/ha to the soil preemergence with chlorsulfuron or postemergence 2 days prior to chlorsulfuron treatment, reverses shoot growth inhibition induced by the herbicide in varying degree in ‘XL25A’ and ‘XL72B’ corn hybrids and ‘FRM017’ and ‘FR619’ inbreds, but not in soybean [Glycine max (L.) Merr., var. ‘Amsoy-71’]. Under similar conditions, flurazole [2-chloro-4-(trifluoromethyl)-5-thiazolecarboxylic acid (phenylmethyl ester)] and CGA-92194 [α-(1,3-dioxolan-2-yl-methoxy)-imino-benzeneacetonitrile] are less effective than R-25788 in protecting corn genotypes from chlorsulfuron injury. R-25788 also partially reverses chlorsulfuron-induced root growth inhibition in XL25A and FR619 corn but not in pea (Pisum sativum L. var. ‘Dwarf Gray Sugar’). Acetohydroxyacid synthase (AHAS) is higher in both activity and the proportion that is very sensitive to in vitro chlorsulfuron inhibition when prepared from XL25A shoots than from the roots. R-25788 does not reverse the in vitro inhibition of corn acetohydroxyacid synthase (AHAS) by chlorsulfuron. Pretreatment of 5-day-old XL25A corn with R-25788 at 24 or 48 μM significantly increases AHAS activity by approximately 25% in both shoots and roots but does not change its in vitro sensitivity to chlorsulfuron. This antidote also increases the glutathione (GSH) content in roots and etiolated shoots. The R-25788-induced elevation of AHAS activity may contribute to its antidotal effect in corn.

Applications of both terbufos and nicosulfuron can result in a synergistic interaction that injures corn. Field studies were conducted at two Illinois locations in 1991 to determine the effect of insecticide formulation and application method on the serverity of this interaction. Terbufos, applied to the soil at planting, interacted with nicosulfuron applied postemergence to injure corn and reduce grain yield. In-furrow-applied terbufos caused a more injurious interaction to corn than terbufos placed in a surface band; the 15G formulation was more injurious than the 20CR formulation. Simulated rainfall timing experiments were conducted in 1992 and 1993 by treating corn with terbufos 15G and terbufos 20CR and applying rainfall (3.8 cm) 1, 7, or 14 d before nicosulfuron application. No visual injury or yield reductions were noted in corn treated with nicosulfuron alone. Terbufos 15G caused greater corn injury than did terbufos 20CR at each rainfall timing when sprayed with nicosulfuron. Corn injury and subsequent grain yield that can result from the interaction between nicosulfuron and terbufos was greater when simulated rainfall occurred 1 and 7 d before nicosulfuron application than when rainfall occurred 14 d before application.

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.

High herbicide costs and uncertainty about annual weed control at planting have limited adoption of no-till spring wheat production systems in the northern Great Plains. Chlorsulfuron, metsulfuron, and CGA-131036 at 10 to 20 g ai ha–1 plus nonionic surfactant generally controlled both emerged kochia and wild mustard equally well (>80%) whether or not combined with glyphosate at 250 g ha–1 plus nonionic surfactant. In two of three trials persistent phytotoxic residues of these sulfonylurea herbicides in soil controlled both weeds better in midseason and early summer 1 yr after treatment than did glyphosate, which has only foliar activity. While the absolute net returns of different treatments varied among herbicides, relative net returns were insensitive to changes in either herbicide or wheat price. Herbicide use tended to boost net returns for no-till spring wheat in years with good weather but depressed net returns in a drought year. Chlorsulfuron at 10 and 20 g ha–1 increased net returns in all three trials. Metsulfuron and combinations of either metsulfuron or chlorsulfuron with glyphosate had variable effects on net returns.

In field experiments conducted near Marianna, Trenton, and Archer, FL in 1990 and 1991, nicosulfuron applied 55 weeks after planting (WAP) at 18, 27, 36, or 54 g ai/ha injured peanut initially. When applied 7 WAP, only the two higher nicosulfuron rates injured peanut more than 10%. By 6 wk after application, crop injury was less than 8% for all treatments, except the highest (54 g/ha) rate. Nicosulfuron applied 5 or 7 WAP at 54 g/ha reduced peanut yield and sound mature kernels.

'Silver Xtra Sweet’, ‘How Sweet It Is', ‘Zenith’ and 'Sweetie 76’ were evaluated for response to 0, 35, and 70 g/ha nicosulfuron applied POST at the 5- to 6- or 7- to 8-leaf stages of growth. Nicosulfuron (35 g/ha) caused 60 to 80% visible injury to Silver Xtra Sweet. How Sweet It Is and Zenith were moderately tolerant (< 20% visible injury) and Sweetie 76 was the most tolerant (10% visible injury). All cultivars were less tolerant when nicosulfuron was applied at the 7- to 8-leaf than the 5- to 6-leaf stage. Plant height of Silver Xtra Sweet was reduced 51% by 35 g/ha nicosulfuron applied at the 5- to 6-leaf stage and injury increased when nicosulfuron was applied at the 7- to 8-leaf stage. Yield losses of Silver Xtra Sweet occurred as a result of the nicosulfuron treatments.

Field experiments were conducted over a 4-yr period, 1989 to 1992, in southern Manitoba to investigate potato (5. tuberosum) response to simulated drift of the dimethylamine salt of dicamba, 2.8 to 22.2 g ai ha–1; alkanolamine salt of clopyralid, 4 to 32 g ai ha–1; and tribenuron, 0.15 to 1.2 g ai ha–1. Rate ranges investigated corresponded to 2 to 16% of the recommended field rate for each herbicide. Dicamba at 22.2 g ai ha–1, clopyralid at 32 g ai ha–1, and tribenuron at 1.2 g ai ha–1 reduced total tuber yields 40, 29, and 41%, respectively, and marketable yields 74, 75, and 53%, respectively. Average weight of marketable-size tubers was unaffected by any treatment in any year. No tuber malformations were observed. Tubers produced on treated plants were planted the year following treatment to investigate the effects of simulated drift on subsequent tuber regrowth. Injury symptoms were evident for each herbicide in 2 out of 3 yr, but neither total nor marketable yields were affected.

Sixteen sweet corn cultivars, representing a range of endosperm genotypes, were evaluated to determine cultivar tolerance to nicosulfuron plus rimsulfuron in greenhouse and field studies conducted over a two-year period. Response to nicosulfuron plus rimsulfuron varied widely, depending on cultivar and application rate. In the field, four cultivars were tolerant to applications of nicosulfuron plus rimsulfuron at rates of 50 g/ha. In the greenhouse, eight cultivars were tolerant to nicosulfuron plus rimsulfuron at 25 g/ha. ‘Merit’ and ‘Silver Extra Sweet’ were most sensitive, with applications of nicosulfuron plus rimsulfuron resulting in death of all plants. ‘Miracle,’ ‘Extra Early Super Sweet,’ ‘Bunker Hill,’ and ‘Sweet Belle’ were tolerant.

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.