Herbicide resistance has for decades been an increasing problem of agronomic crops such as corn and soybean. Several weed species have evolved herbicide resistance in turfgrass systems such as golf courses, sports fields, and sod production—particularly biotypes of annual bluegrass and goosegrass. Consequences of herbicide resistance in agronomic cropping systems indicate what could happen in turfgrass if herbicide resistance becomes broader in terms of species, distribution, and mechanisms of action. The turfgrass industry must take action to develop effective resistance management programs while this problem is still relatively small in scope. We propose that lessons learned from a series of national listening sessions conducted by the Herbicide Resistance Education Committee of the Weed Science Society of America to better understand the human dimensions affecting herbicide resistance in crop production provide tremendous insight into what themes to address when developing effective resistance management programs for the turfgrass industry.

Reductions in MSMA use for weed control in turfgrass systems may have led to increased common carpetgrass infestations. The objective of our research was to identify alternative POST herbicides for control of common carpetgrass using field and controlled-environment experiments. Field applications of MSMA (2.2 kg ai ha−1) and thiencarbazone + iodosulfuron + dicamba (TID) (0.171 kg ai ha−1) resulted in the greatest common carpetgrass control 8 wk after initial treatment (WAIT): 94% and 91%, respectively. Thiencarbazone + foramsulfuron + halosulfuron (TFH) (0.127 kg ai ha−1) applied in the field resulted in 77% control 8 WAIT, whereas all other treatments were ≤19% effective at 8 WAIT. All treatments resulted in greater common carpetgrass control when applied in the greenhouse. Applications of MSMA, TFH, and TID resulted in the highest common carpetgrass control in the greenhouse 8 WAIT: 94%, 94%, and 91%, respectively. Control with nicosulfuron (0.035 kg ai ha−1) and trifloxysulfuron (0.028 kg ai ha−1) (81% and 75%, respectively) was greater in the greenhouse than observed in the field 8 WAIT. Sequential applications of foramsulfuron (0.058 kg ai ha−1) resulted in only ≤11% common carpetgrass control 8 WAIT, regardless of application site. All herbicide treatments in the greenhouse resulted in reduced aboveground common carpetgrass biomass 8 WAIT compared to the nontreated control (12.9 g). Aboveground biomasses of common carpetgrass in response to MSMA, TID, TFH, nicosulfuron, and trifloxysulfuron were 1.6 to 2.1 g, regardless of treatment. Reduced efficacy of foramsulfuron was reflected in greater biomass (4.7 g) in response to treatments. Thiencarbazone + iodosulfuron + dicamba may be an alternative to MSMA for common carpetgrass control; however, long-term assessment may be warranted to evaluate treatment effectiveness. Further investigation into application timing may be necessary to enhance the efficacy of TFH for the control of common carpetgrass.

Doveweed is a problematic weed of lawns and sod production, as well as golf course roughs, fairways, and tees. End-user reports of selective POST control options are inconsistent and control is often short-lived. In addition, inconsistent control with non-selective herbicides such as glyphosate is common. The goals of this research were: (1) evaluate selective POST doveweed control options in ‘Tifway’ hybrid bermudagrass turf; (2) compare efficacy of single vs. sequential applications of selective POST herbicides; (3) quantify doveweed tolerance to glyphosate; and (4) quantify recovery of foliar applied glyphosate following treatment with a C14-glyphosate solution. A single application of sulfentrazone+metsulfuron; thiencarbazone+iodosulfuron+dicamba or 2,4-D+MCPP+dicamba+carfentrazone; or thiencarbazone+foramsulfuron+halosulfuron provided >60% control 2 weeks after initial treatment (WAIT). A second application of these treatments 3 WAIT improved control 6 WAIT. Two applications of 2,4-D+MCPP+dicamba+carfentrazone or thiencarbazone+foramsulfuron+halosulfuron provided ~80% control 6 WAIT. Doveweed was tolerant to glyphosate application up to 5.68 kgaeha-1. Absorption of 14C-glyphosate was compared between doveweed with cuticle intact, doveweed with a disturbed cuticle, and smooth crabgrass. 14C-glyphosate recovery from the leaf surface of doveweed plants with an intact cuticle was 93.6%. In comparison, 14C-glyphosate recovery from the leaf surface of doveweed plants with a disrupted cuticle and the leaf surface of crabgrass plants was 79.1 and 70.5%, respectively.

Turfgrass managers currently have few readily available means of evaluating herbicide resistance in annual bluegrass during the growing season. Research was conducted to determine if agar-based diagnostic tests developed for agronomic weeds could be used to reliably confirm herbicide resistance in annual bluegrass harvested from golf course turf. Annual bluegrass phenotypes with target-site resistance to acetolactate synthase (ALS; R3, R7), enolpyruvylshikimate-3-phosphate synthase (EPSPS; R5), and photosystem II (PSII; R3, R4) inhibiting herbicides were included in experiments along with an herbicidal susceptible phenotype (S). Single tiller plants were washed free of soil and transplanted into autoclavable polycarbonate plant culture boxes filled with plant tissue culture agar amended with a murashigee-skoog medium and trifloxysulfuron (6.25, 12.5, 25, 50, 75, 100, or 150 μM), glyphosate (0, 6, 12, 25, 50, 100, 200, or 400 μM), or simazine (0, 6, 12, 25, 50, 100, 200, or 400 μM). Mortality in agar was assessed 7 to 10 days after treatment (depending on herbicide) and compared to responses observed after treating individual plants of each phenotype with trifloxysulfuron (28 g ai ha-1), glyphosate (1120 g ae ha-1), or simazine (1120 g ai ha-1) in an enclosed spray chamber. Fisher’s exact test (α = 0.05) determined that mortality in agar with 12.5 μM trifloxysulfuron and 100 μM glyphosate was not significantly different than treating whole plants via traditional spray application. Mortality with all concentrations of simazine in agar was significantly different than that observed after treating resistant and susceptible phenotypes via traditional spray application. Our findings indicate that an agar-based diagnostic assay can be used to detect annual bluegrass resistance to ALS- or EPSPS-inhibiting herbicides in less than 10 days; however, additional research is needed to refine this assay for use with PSII-inhibiting herbicides.

Torpedograss has invaded fine turfgrasses in the Southern U.S. due to its tolerance to most commonly used turfgrass herbicides. Research was conducted to determine torpedograss and ‘Tifway’ bermudagrass tolerance to quinclorac and tank-mix combinations with other turf herbicides. Quinclorac rates in excess of 2.2 kg ai/ha were required for control (≥ 80%) of torpedograss. Sequential applications were more effective than single applications. Generally, sequential applications made 3 wk after the initial were more effective than delaying sequential applications until 4 wk after the initial application. Tifway bermudagrass injury from quinclorac applied at 4.5 kg/ha, or at 2.2 kg/ha followed by a sequential application of 1.1 or 2.2 kg/ha, was observed at 4 to 10 wk; however, turf recovered thereafter. Sequential applications of quinclorac plus imazaquin (1.1 + 0.6 kg/ha) increased torpedograss control (approximate 35%) as compared to quinclorac plus MSMA (1.1 + 1.1 kg/ha) but also decreased turf quality versus quinclorac applied alone or in combination with MSMA. Quinclorac applied at 2.2 kg/ha followed by 1.1 kg/ha applied 3 or 6 wk after the initial controlled torpedograss best with least reduction in bermudagrass quality. Quinclorac is the first herbicide reported to selectively control torpedograss in bermudagrass turf.

Methiozolin is an isoxazoline herbicide being investigated for selective POST annual bluegrass control in managed turfgrass. Research was conducted to evaluate methiozolin efficacy for controlling two annual bluegrass phenotypes with target-site resistance to photosystem II (PSII) or enolpyruvylshikimate-3-phosphate synthase (EPSPS)-inhibiting herbicides (i.e., glyphosate), as well as phenotypes with multiple resistance to microtubule and EPSPS or PSII and acetolactate synthase (ALS)-inhibiting herbicides. All resistant phenotypes were established in glasshouse culture along with a known herbicide-susceptible control and treated with methiozolin at 0, 125, 250, 500, 1000, 2000, 4000, or 8000 g ai ha−1. Methiozolin effectively controlled annual bluegrass with target-site resistance to inhibitors of EPSPS, PSII, as well as multiple resistance to EPSPS and microtubule inhibitors. Methiozolin rates required to reduce aboveground biomass of these resistant phenotypes 50% (GR50 values) were not significantly different from the susceptible control, ranging from 159 to 421 g ha−1. A phenotype with target-site resistance to PSII and ALS inhibitors was less sensitive to methiozolin (GR50=862 g ha−1) than a susceptible phenotype (GR50=423 g ha−1). Our findings indicate that methiozolin is an effective option for controlling select annual bluegrass phenotypes with target-site resistance to several herbicides.

Poor annual bluegrass control was reported in golf course roughs following treatment with prodiamine (1120 gaiha−1) and glyphosate (840 gaeha−1) during hybrid bermudagrass dormancy. Research was conducted to determine if this annual bluegrass phenotype was resistant to both prodiamine and glyphosate and to determine the efficacy of herbicide mixtures for controlling this phenotype in the field. In PRE or POST dose-response experiments, 9 to 31 times more prodiamine or glyphosate was needed to control (or reduce dry biomass of) this resistant phenotype by 50% compared to an herbicide-susceptible phenotype. Moreover, glyphosate-susceptible plants accumulated 50% more shikimic acid (898 mgkg−1) 6 d after treatment than those resistant to glyphosate (394 mgkg−1). October (fall) applications of herbicide mixtures containing trifloxysulfuron, simazine, S-metolachlor, or mesotrione controlled this resistant annual bluegrass phenotype 84 to 98% in April (spring), with no differences detected among treatments. Our findings document the second instance of annual bluegrass evolving multiple resistance in a managed turfgrass system. However, several herbicide mixtures can be used to effectively manage this resistant phenotype.

Options for suppressing bermudagrass seedheads in managed turfgrass systems are limited. Experiments were conducted in 2009 and 2010 evaluating the use of fenoxaprop (25, 50, 75, and 100 g ha−1) for ‘Riviera’ bermudagrass seedhead suppression and growth regulation compared to imazapic (52 g ha−1), trinexapac-ethyl (91 g ha−1) and mefluidide (561 g ha−1). In field experiments, seedhead suppression ranged from 77 to 100% for fenoxaprop and imazapic at 35 d after treatment (DAT). Comparatively, seedhead suppression was < 25% for either trinexapac-ethyl or mefluidide at 35 DAT. Seedhead suppression was > 90% from 7 to 35 DAT for fenoxaprop applied at ≥ 50 g ha−1. Injury, determined visually, from fenoxaprop and imazapic in both the field and greenhouse measured < 25% on all rating dates, with no significant injury present after 21 DAT. In greenhouse experiments, fenoxaprop and trinexapac-ethyl showed similar reductions of bermudagrass growth; no differences in aboveground biomass were detected between these treatments at 42 DAT. Results of the current study illustrate that fenoxaprop and imazapic can be applied for bermudagrass seedhead suppression and growth regulation if moderate (< 25%) injury can be tolerated up to 21 DAT. Additional research is needed to evaluate the use of fenoxaprop and imazapic for seedhead suppression on other common and hybrid bermudagrasses.

Ground ivy and khakiweed are troublesome broadleaf weeds of warm-season turfgrass. Field studies were conducted in Tennessee (TN) and Texas (TX) from 2008 to 2010 to evaluate the efficacy of sulfentrazone plus metsulfuron and carfentrazone plus metsulfuron tank mixtures compared with metsulfuron alone for control of ground ivy and khakiweed. In TN, sulfentrazone plus metsulfuron and carfentrazone plus metsulfuron provided accelerated control of ground ivy compared with metsulfuron alone. Over a 2-yr period, ground ivy control with metsulfuron at 10, 21, and 42 g ai ha−1 ranged from 0 to 5% 7 d after treatment (DAT) and 12 to 60% 14 DAT. Ground ivy control with mixtures of sulfentrazone plus metsulfuron ranged from 40 to 72% 7 DAT and 87 to 100% 14 DAT. Similarly, carfentrazone plus metsulfuron controlled ground ivy 5 to 32% 7 DAT and 23 to 93% 14 DAT. In TX, carfentrazone plus metsulfuron and sulfentrazone plus metsulfuron controlled khakiweed greater than metsulfuron alone 7 and 14 DAT as well. Few differences in ground ivy and khakiweed control were detected 56 DAT because metsulfuron applied alone at 21 g ai ha−1 controlled both weeds > 77%, similar to each mixture. These data indicate that when applied in mixtures, sulfentrazone and carfentrazone accelerate ground ivy and khakiweed control with metsulfuron but do not affect long-term efficacy.

Acetolactate synthase–- (ALS-) inhibiting herbicides are frequently used to control annual bluegrass in managed turfgrass systems. Recently, the number of annual bluegrass populations resistant to these herbicides has increased on golf courses. Previous research involving annual bluegrass resistance to ALS inhibitors has included elucidating the mechanism of resistance and in vivo response of ALS to ALS-inhibiting herbicides. The purpose of this research was to generate baseline information on enzymatic parameters of resistant (R) and susceptible (S) annual bluegrass biotypes and further distinguish these biotypes by comparing vegetative growth and reproductive characteristics. The R biotype contained a mutation in the ALS gene resulting in a Trp574 to Leu amino acid substitution. Compared to the S biotype, the R biotype exhibited a 27- and 10-fold resistance to trifloxysulfuron at the whole-plant level and under in vitro conditions, respectively. No significant differences were observed in substrate concentration at one-half maximum rate of enzyme activity (pyruvate) or extractable ALS activity between biotypes, but the maximum rate of enzyme activity was higher for the R biotype. The feedback inhibition of ALS activity by the branched-chain amino acids was higher for the R biotype than the S biotype, with leucine, valine, and isoleucine inhibiting ALS activity 20, 6, and 4% more in the R biotype, respectively. The R biotype produced more inflorescences and seeds per plant in comparison with the S biotype, but relative growth rates between biotypes were similar at all harvest intervals. Our research provides baseline information regarding ALS enzyme response, vegetative growth, and reproductive characteristics of annual bluegrass biotypes resistant and susceptible to ALS-inhibiting herbicides.

Glyphosate is used in the transition zone to control annual bluegrass in fully dormant warm-season grasses. A suspected resistant (R) biotype of annual bluegrass was identified on a golf course in South Carolina after at least 10 consecutive years of glyphosate application. Greenhouse bioassays revealed the R biotype was 4.4-fold resistant to glyphosate compared with a standard susceptible (S) biotype. Further studies were conducted to investigate the mechanism conferring glyphosate resistance in the R biotype. Leaf discs of both biotypes accumulated shikimate in response to increasing glyphosate concentration, but the glyphosate concentration resulting in 50% EPSP synthase inhibition as a result of shikimate accumulation (I50) was 4.2-fold higher in the R biotype compared with the S biotype. At the whole plant level, similar levels of shikimate accumulation were observed between biotypes at 6 and 24 h after treatment (HAT) with glyphosate, but greater shikimate accumulation occurred in the S biotype at 72, 120, and 168 HAT. Shikimate levels decreased in the R biotype after 72 HAT. There were no differences in 14C-glyphosate absorption between biotypes. However, more 14C-glyphosate translocated out of the treated leaf in the R biotype and into root tissues over time compared with the S biotype. Partial sequencing of the EPSP synthase gene revealed a point mutation that resulted in an Ala substitution at Pro106. Although other mechanisms may contribute to glyphosate resistance, these results confirm a Pro106 to Ala substitution is associated with resistance to glyphosate in the R annual bluegrass biotype.

Annual bluegrass is the most problematic winter annual weed in managed turfgrass. Acetolactate synthase (ALS)-inhibiting herbicides are effective for annual bluegrass control, but reliance on this mode of action can select for herbicide-resistant biotypes. Two annual bluegrass biotypes not controlled with ALS-inhibiting herbicides were reported at golf courses in South Carolina and Georgia. Research was initiated at Clemson University to verify the level of resistance of these biotypes to ALS inhibitors. Two ALS-susceptible (S) and suspected resistant (SCr, GAr) annual bluegrass biotypes were established in a greenhouse. Dose-response experiments were conducted on mature annual bluegrass plants using trifloxysulfuron, foramsulfuron, and bispyribac-sodium, all ALS-inhibiting herbicides. Additionally, a rapid diagnostic ALS activity assay was optimized and conducted using the same herbicides. For dose-response experiments, the rate of herbicide that reduced shoot biomass 50% (I50) values for the S biotypes were 13.6 g ai ha−1 for trifloxysulfuron, 7.0 g ai ha−1 for foramsulfuron, and 38.3 g ai ha−1 for bispyribac-sodium. Fifty percent shoot biomass reduction was not observed in either the SCr or GAr biotypes at eight times the labeled field rate of all ALS-inhibiting herbicides tested. For in vivo tests of ALS activity, the SCr biotype yielded I50 (concentration of herbicide that reduced ALS activity 50%) values 3,650, 3,290, and 13 times the S biotypes following treatment with trifloxysulfuron, foramsulfuron, and bispyribac-sodium, respectively. Similarly, I50 values for the GAr biotype were 316, 140, and 64 times greater than the S biotypes following the same herbicide treatments. This research indicates high levels of annual bluegrass resistance to multiple ALS-inhibiting herbicides in South Carolina and Georgia. Future research should focus on the mechanisms of ALS resistance in these annual bluegrass biotypes as well as alternative options for control not targeting the ALS enzyme.

Annual bluegrass is one of the most diverse plant species in the world and is the most problematic winter annual weed in commercial turfgrass. Continuous application of the same herbicide mechanism of action for annual bluegrass control on golf courses has increased herbicide-resistant populations. The purpose of this research was to simulate six herbicide-use strategies to evaluate the risk of annual bluegrass resistance evolution to glyphosate. In a worst-case scenario of yearly glyphosate applications at dormancy, resistance evolved within 10 yr and was predicted to evolve in > 90% of populations by yr 20. When glyphosate was rotated on alternate years with a unique mechanism of action, resistance was delayed for 12 to 15 yr. Season-long control of annual bluegrass often requires multiple herbicide applications. Therefore, additional strategies were simulated in which glyphosate was applied at dormancy with combinations of PRE and/or POST herbicides at various timings. Resistance was most effectively delayed with a PRE application in late summer, a POST application in fall, and alternating glyphosate with a different POST option at dormancy. This delayed resistance by 25 yr and a 35% risk was predicted after 50 yr. Strategies utilizing three annual herbicide applications with unique mechanisms of action were more effective for controlling population growth compared to other strategies. Resistance was predicted to evolve within 35 yr for each of the strategies simulated. However, these results indicate annual bluegrass herbicide resistance can be managed by using an integrated herbicide program, rotating unique mechanisms of action as frequently as possible.

Glyphosate is regularly used to control annual bluegrass populations in dormant bermudagrass turf. A population of annual bluegrass not controlled by glyphosate at 840 g ha−1 (glyphosate resistant, GR) was identified on a golf course in Humboldt, TN in 2010. Mature tillers of GR plants were established in a greenhouse and treated with glyphosate at 0, 210, 420, 840, 1,680, 3,360, and 6,720 g ha−1. Mature tillers of a biotype known to be susceptible to glyphosate (SS) were also established in the greenhouse and subjected to the same treatments. At 14 d after treatment (DAT), glyphosate controlled the SS biotype > 95% at rates > 420 g ha−1. Comparatively, the GR biotype was only controlled 76% with glyphosate at 6,720 g ha−1. The rates required to provide 50% control (I50 values) for SS and GR biotypes were 236 and 2,812 g ha−1 respectively, resulting in a resistance factor of 12. Photochemical efficiency (Fv/Fm) values on SS plants treated with glyphosate at > 210 g ha−1 measured 0.000 at 14 DAT, whereas Fv/Fm values on GR plants were not significantly different from the untreated control with glyphosate rates ≤ 840 g ha−1 on the same date. In laboratory experiments, the SS biotype accumulated greater shikimate concentrations than the GR biotype 3 to 6 DAT. Future research should evaluate strategies for managing GR and SS annual bluegrass with alternative modes of action.

Indaziflam controls annual grassy weeds by inhibiting cellulose biosynthesis. Research was conducted from 2008 to 2011 in Tennessee, Texas, and Georgia evaluating the efficacy of indaziflam for PRE and POST control of annual bluegrass in bermudagrass turf. In Texas, indaziflam at 30, 40, 50, and 60 g ai ha−1 applied PRE provided 93 to 100% annual bluegrass control through 28 wk after treatment. When applied PRE at 80 g ai ha−1 and at 4, 8, and 12 wk after PRE (WAP), indaziflam controlled annual bluegrass 67 to 100% 32 wk after initial treatment (WAIT) in Tennessee; however, reduced efficacy was observed with 12 WAP treatments in a single year of a 2-yr study. Similarly, annual bluegrass control with PRE applications or with 4 and 8 WAP applications of indaziflam at 35 and 52.5 g ai ha−1 ranged from 88 to 100% at 30 WAIT in Tennessee. In Georgia, these rates of indaziflam applied PRE and 4 WAP controlled annual bluegrass 96 to 100% on all evaluation dates and resulted in 97 to 100% reduction in plant counts relative to the untreated control at 30 WAIT. When applied 8 WAP, the 35 and 52.5 g ai ha−1 rates of indaziflam controlled annual bluegrass only 51 to 71% at 30 WAIT in Georgia. Although increasing the application rate of indaziflam treatments 8 WAP provided greater annual bluegrass control, each rate provided significantly lower control when applied 8 WAP compared with PRE or at 4 WAP. No bermudagrass injury was observed in this research. Results suggest indaziflam provides effective PRE and early POST control of annual bluegrass in bermudagrass turf. However, additional research is needed to determine the effects of plant size and maturity on indaziflam efficacy for POST annual bluegrass control.

Field studies were conducted to evaluate foramsulfuron for postemergence control of goosegrass in bermudagrass turf as a possible replacement for MSMA. In field trials on a golf course and sports fields planted to bermudagrass, mature goosegrass was controlled effectively (>85% goosegrass dead on the basis of canopy area) with two applications of foramsulfuron plus metribuzin. The herbicide rates that were effective varied among studies, e.g., foramsulfuron at 0.029 or 0.044 kg ai/ha mixed with metribuzin at 0.105 to 0.210 kg ai/ha. Goosegrass was often controlled with MSMA at 2.24 kg ai/ha plus metribuzin at 0.105 to 0.210 kg/ha, but foramsulfuron was always as effective, or more effective, than MSMA, in controlling mature goosegrass, at the same rate of metribuzin. Bermudagrass phytotoxicity of foramsulfuron plus metribuzin was temporary and not different from MSMA plus metribuzin. In one location there was noticeable phytotoxicity 4 wk after initial treatment.

Two field experiments were conducted to evaluate the reduction of torpedograss canopy by multiple split applications of quinclorac applied postemergence (POST) to bermudagrass golf course roughs in Florida. In one experiment, quinclorac treatments were reapplied for a second year to the same plots, followed by biomass harvest, to evaluate the reduction of torpedograss rhizomes. Quinclorac sprayed at 1.68 kg/ha/yr visually reduced torpedograss canopy to a varying extent, depending on the number of split applications. The most effective treatment, 0.42 kg/ha quinclorac applied four times each year for 2 yr, reduced torpedograss canopy to 10% compared with 86% torpedograss canopy in the untreated plots, and reduced torpedograss dry weight to 1,570 kg/ha compared with 8,010 kg/ha in the untreated plots. After reapplication for 2 yr with the commercially labeled treatment, quinclorac at 0.84 kg/ha applied twice per year, torpedograss canopy was reduced to 45% and dry weight to 4,640 kg/ha. Visual evaluation of canopy was too optimistic in representing the herbicidal control of torpedograss by quinclorac because torpedograss regrew from rhizomes, and canopy was a relatively small part of the plant. In plots not chemically treated, pachymorph rhizomes were 63%, leptomorph rhizomes were 24%, and leaves were only 13% of the total dry weight of torpedograss.

Several field studies have observed increased foramsulfuron efficacy for the control of dallisgrass when foramsulfuron is applied after MSMA. Therefore, laboratory studies were conducted with mature dallisgrass to study the absorption and translocation of 14C-foramsulfuron, and then examine the impact of preliminary applications (preapplications) of MSMA or foramsulfuron on herbicide absorption and movement. Herbicide absorption increased rapidly through 4 h, and by 8 h, differences in absorption between pretreated and control plants were evident. After 48 h, foramsulfuron absorption in non-pretreated plants was 55%, whereas plants that received either pretreatment absorbed 70% of the herbicide. Translocation above (younger tissue) and below (older tissue) the treated leaf was 0.65 and 0.62% for non-pretreated plants, respectively. Pretreatment with foramsulfuron resulted in the translocation of 2.12 and 1.55% of applied radioactivity above and below the treated leaf, respectively. Pretreatment with MSMA resulted in the translocation of 2.33 and 2.34% of applied radioactivity above and below the treated leaf, respectively. These data indicated that pretreatment of mature dallisgrass with either foramsulfuron or MSMA results in an increase in both uptake and translocation of foramsulfuron applied 2 wk after pretreatment. The increase in absorption and translocation of foramsulfuron in the pre–MSMA-treated plants may explain the increase in control observed in the field when comparing it to the pre–foramsulfuron-treated dallisgrass plants.

Purple nutsedge response to various rates and timings of imazosulfuron was evaluated in 2007 and 2008 in Abilene, TX. Bermudagrass phytotoxicity never exceeded 4% throughout the duration of the trial and all bermudagrass recovered within 7 d of herbicide application. Imazosulfuron (0.56 kg ai ha−1) followed by (fb) imazosulfuron 1 wk after initial treatment (WAIT), imazosulfuron at 1.12 kg ai ha−1, and trifloxysulfuron at 0.03 kg ai ha−1 exhibited 94 to 96% control 4 WAIT. Imazosulfuron (0.56 kg ai ha−1) fb imazosulfuron 2, 3, and 4 WAIT exhibited 99% control 4 WAIT. Eight weeks later (12 WAIT), imazosulfuron (0.56 kg ai ha−1) fb imazosulfuron 3 WAIT controlled purple nutsedge 91%, whereas similar control (82 to 84%) was observed with a single application of trifloxysulfuron and imazosulfuron (0.56 kg ai ha−1) fb imazosulfuron 2 and 4 WAIT. A single application of imazosulfuron at 1.12 kg ai ha−1 and sequential treatment with imazosulfuron (0.56 kg ai ha−1) on a 1-wk interval only controlled purple nutsedge 51 to 69% 12 WAIT. Timing of sequential imazosulfuron application was identified as an important component of the purple nutsedge control program. Waiting 2, 3, or 4 WAIT for sequential imazosulfuron applications, rather than 1 WAIT, increased purple nutsedge control 31 to 40% 12 WAIT. The highest level of purple nutsedge control (91%) was observed with applications of imazosulfuron (0.56 kg ai ha−1) fb imazosulfuron 3 WAIT applied during midsummer. However, control with this treatment was statistically similar to control with a single application of trifloxysulfuron (82%).

Bermudagrass is a troublesome weed of zoysiagrass golf-course fairways. Field research was conducted in 2009 and 2010 evaluating bermudagrass suppression with applications of fluazifop plus triclopyr at various timings. Three rates of fluazifop (0.10, 0.21, and 0.32 kg ai ha−1) were applied with triclopyr (1.12 kg ae ha−1) once six thresholds of growing-degree-day accumulation (GDD10C) had been reached: 200, 450, 825, 1,275, 1,775, and 2,250 GDD10C. Yearly accumulated GDD10C values were calculated with a base temperature of 10 C beginning on 1 January. Applications at 200 and 2,250 GDD10C suppressed bermudagrass ≥ 90% at 5 WAT each year. Increased rates of fluazifop did not provide additional bermudagrass suppression at these timings. Cooling accumulation models may be needed to time fall applications, as the 1,775 GDD10C timing in 2009 provided similar bermudagrass suppression to the 2,250 GDD10C timing in 2010. Late-spring and midsummer applications at 450 GDD10C, 825 GDD10C, and 1,275 GDD10C only suppressed bermudagrass 4 to 16% at 6 wk after treatment (WAT) in 2009 and 0 to 57% at 6 WAT in 2010. Zoysiagrass injury measured < 25% for all timings and decreased to 0 to 7% by 5 WAT each year. Future studies should evaluate bermudagrass suppression with other herbicides with the use of growing-degree-day and cooling accumulation models.