Surveys were conducted across the northern Great Plains of Canada in 1996 and 1997 to determine the nature and occurrence of herbicide-resistant (HR) biotypes of wild oat (Avena fatua). The surveys indicated that resistance to acetyl-CoA carboxylase (ACCase) inhibitors (Group 1) occurred most frequently relative to other herbicide groups. Group 1-HR wild oat occurred in over one-half of fields surveyed in each of the three prairie provinces. Of particular concern was the relatively high incidence of multiple-group resistance in wild oat in Saskatchewan and Manitoba. In Saskatchewan, 18% of Group 1-HR populations were also resistant to acetolactate synthase inhibitors (imidazolinones), even though these herbicides were not frequently used. In Manitoba, 27% of fields surveyed had wild oat resistant to herbicides from more than one group. Four populations were resistant to all herbicides registered for use in wheat (Triticum aestivum). Depending on the nature of resistance in wild oat, alternative herbicides available for their control may substantially increase costs to the grower. The cost to growers of managing HR wild oat in Saskatchewan and Manitoba using alternative herbicides is estimated at over $4 million annually. For some HR biotypes, alternative herbicides either are not available or all have the same site of action, which restricts crop or herbicide rotation options and threatens the future sustainability of small-grain annual cropping systems where these infestations occur.

In Saskatchewan, a field survey was conducted in 1996 and a grain elevator survey in 1997 to determine the nature and occurrence of herbicide-resistant (HR) biotypes of green foxtail (Setaria viridis). Based on results of the field survey, one in every 20 fields (1 million ha) in Saskatchewan is estimated to have acetyl-CoA carboxylase (ACCase) inhibitor (Group 1)-HR green foxtail. Of the samples received from 30 grain elevators, 83% had Group 1 resistance. Similar to the field survey, incidence of aryloxyphenoxy propionate (AOPP) resistance was much higher than cyclohexanedione (CHD) resistance. Both surveys indicated relatively low incidence of dinitroaniline (Group 3) resistance or cross-resistance (Groups 1 and 3). Most alternative herbicides to control Group 1-HR green foxtail in broadleaf crops and cross-HR biotypes in cereal and broadleaf crops increase costs to the grower.

Field, greenhouse, and laboratory studies were conducted to examine the potential for antagonism of postemergence graminicides when tank-mixed with cloransulam and to determine the role of herbicide absorption and translocation in observed antagonistic responses. Cloransulam antagonized annual grass control with aryloxyphenoxypropionate herbicides fluazifop-P, quizalofop, and the prepackaged formulation of fluazifop-P plus fenoxaprop. Cloransulam did not affect annual grass control with the cyclohexandiones clethodim and sethoxydim. In the greenhouse, increasing the rate of the graminicides was a more effective strategy for overcoming antagonism for quizalofop than for fluazifop-P or fluazifop-P plus fenoxaprop, and success was species dependent. Annual grass control with clethodim, sethoxydim, and glyphosate was not adversely affected by tank mixtures with cloransulam. Control of large rhizome johnsongrass was initially reduced when cloransulam was mixed with sethoxydim, fluazifop-P plus fenoxaprop, or quizalofop. By 6 wk after treatment, control of rhizome johnsongrass was antagonized only when cloransulam was mixed with sethoxydim. Rainfall within 1.5 h of application reduced johnsongrass control with glyphosate and sethoxydim but did not affect activity of the other herbicides. Absorption of 14C-fluazifop-P and 14C-quizalofop into broadleaf signalgrass was not affected by cloransulam 6 or 24 h after treatment. Translocation of 14C-fluazifop-P to broadleaf signalgrass shoot tissue above and below the treated leaf was decreased when fluazifop-P was combined with cloransulam. Translocation of quizalofop was not affected by cloransulam.

A diagnostic test (Syngenta Quick-Test, QT) used for testing grass weed survivors to herbicides in the field for resistance was evaluated. Cuttings from grass weeds were transplanted into pots to regenerate new leaves, then treated with herbicide. In greenhouse experiments, resistance of known herbicide-resistant blackgrass biotypes to the aryloxyphenoxypropanoate herbicides CGA 184927 and fenoxaprop-ethyl and to the phenylurea herbicide isoproturon was verified by the QT. The findings were similar to those for seedlings grown from seed. Rigid ryegrass from suspect resistant fields in South Australia was sampled and sent by post to Switzerland for QT analysis. Resistance was confirmed in less than 4 wk, which verified resistance as responsible for the field failures. The added features of the QT over current resistance tests suggest a likely fit for in-season testing of surviving weeds and possible follow-up action.

Field and greenhouse dose-response experiments were conducted to investigate the potential for resistance in a johnsongrass biotype from New Kent County, VA that survived repeated applications of quizalofop and quizalofop-P. During 1996 and 1997, foliar injury (30 to 60%) was initially observed on the johnsongrass at the New Kent field site, but this biotype eventually recovered and survived applications of fluazifop-P, quizalofop-P, and sethoxydim at twice the recommended field use rates. However, applications of clethodim at twice the recommended field use rates during 1997 provided essentially complete control of the New Kent johnsongrass biotype. In greenhouse dose-response experiments, the amount of quizalofop-P required to inhibit shoot growth by 50% (GR50) was 13.6 g/ha in the New Kent johnsongrass biotype and 0.8 g/ha in the susceptible johnsongrass biotype. In response to sethoxydim, the GR50 for the New Kent biotype was 122.5 g/ha while that of the susceptible biotype was 21.6 g/ha. Additionally, the New Kent biotype was least sensitive to fluazifop-P, which provided a GR50 value of 148.7 g/ha for the New Kent biotype and 5.1 g/ha for the susceptible biotype. As in the field trials, the New Kent biotype was sensitive to clethodim, which provided a GR50 value of 49.8 g/ha and 69.1 g/ha for the susceptible biotype. These values indicate that the New Kent biotype was 17 times more resistant to quizalofop-P, 5.7 times more resistant to sethoxydim, and 29.5 times more resistant to fluazifop-P than the susceptible biotype, and that the New Kent and susceptible johnsongrass biotypes are equally sensitive to clethodim. These GR50 values for the New Kent johnsongrass biotype are inconsistent with the much higher GR50 values most commonly observed in graminicide-resistant weed biotypes, and suggest a mechanism of resistance other than an insensitive ACCase in the New Kent johnsongrass biotype.

A survey conducted across agricultural ecoregions of Saskatchewan in 1996 revealed that wild oat (Avena fatua) populations resistant to acetyl-CoA carboxylase (ACCase) inhibitors were present in approximately 10% of Saskatchewan fields (2.4 million ha). In the Aspen Parkland and Boreal Transition ecoregions, this increased to 17%. The objective of this study was to determine if agronomic practices promoted or delayed resistance and to assess producer awareness of herbicide resistance. Weed resistance and management questionnaire data from the 1996 resistance survey and management questionnaire data from the 1995 Saskatchewan weed survey were submitted to multiway frequency analysis. The frequency of occurrence of herbicide-resistant wild oat was related directly to ACCase inhibitor use. Resistance to cyclohexanedione (CHD) herbicides was not related to CHD use but to frequency of ACCase inhibitor use (i.e., CHD + aryloxyphenoxypropanoate [AOPP]), suggesting that the pressure imposed by AOPPs contributed to the selection of CHD resistance in wild oat. ACCase inhibitor use was more extensive in the Aspen Parkland and Boreal Transition ecoregions than in the Mixed and Moist Mixed Grassland ecoregions. Crop rotations were not conducive to rotation of herbicides with different sites of action. Frequency of ACCase inhibitor use increased with frequency of annual crops, in spite of the inclusion of cereal and dicot crops in the rotation. Producers utilizing conservation tillage practices in the Grassland ecoregions used proportionally more ACCase inhibitors than those using conventional tillage practices. This increase in ACCase use in conservation tillage systems did not result in an increased incidence of wild oat populations resistant to ACCase inhibitors. Producers reporting troublesome wild oat populations tended to have proportionally more ACCase-resistant wild oat. Producers who reported practicing weed sanitation were less likely to have resistant wild oat than those who were less careful. Increased awareness and implementation of management practices that will reduce the dependency on ACCase herbicides are required to better enable producers to prevent, delay, or manage herbicide-resistant wild oat populations.

Greenhouse studies verified that smooth crabgrass from a golf course tee in southern New Jersey was resistant to fenoxaprop-P, although smooth crabgrass from a nearby untreated rough was susceptible to this herbicide. Fenoxaprop-P-resistant plants were injured, however, when fenoxaprop-P was applied at levels above the maximum use rate for turf. Fenoxaprop-P applied postemergence at 0.76 kg ai/ha, four times the maximum rate, reduced shoot weight of the resistant biotype by 35%, whereas application of 1.52 kg/ha, eight times the maximum rate, reduced shoot weight by 64%. Large crabgrass and the susceptible biotype of smooth crabgrass were controlled by fenoxaprop-P applied at 0.1 kg/ha. Fenoxaprop-susceptible and -resistant biotypes of smooth crabgrass had a similar response to MSMA, dithiopyr, and quinclorac applied postemergence. The fenoxaprop-P–resistant smooth crabgrass biotype was controlled by the cyclohexanedione herbicides sethoxydim and clethodim, but the aryloxyphenoxypropionate herbicides fluazifop and quizalofop reduced shoot weight by only 15 to 66% depending on herbicide and rate.

In input-intensive cropping systems around the world, farmers rarely proactively manage weeds to prevent or delay the selection for herbicide resistance. Farmers usually increase the adoption of integrated weed management practices only after herbicide resistance has evolved, although herbicides continue to be the dominant method of weed control. Intergroup herbicide resistance in various weed species has been the main impetus for changes in management practices and adoption of cropping systems that reduce selection for resistance. The effectiveness and adoption of herbicide and nonherbicide tactics and practices for the proactive and reactive management of herbicide-resistant (HR) weeds are reviewed. Herbicide tactics include sequences and rotations, mixtures, application rates, site-specific application, and use of HR crops. Nonherbicide weed-management practices or nonselective herbicides applied preplant or in crop, integrated with less-frequent selective herbicide use in diversified cropping systems, have mitigated the evolution, spread, and economic impact of HR weeds.

A seedling bioassay was developed for the rapid diagnosis of resistance to clethodim and fluazifop-P in johnsongrass. The assay was based on differences in the coleoptile length of susceptible (S) and resistant (R) seedlings exposed to clethodim and fluazifop-P in petri dishes for 5 d. Bioassay concentrations of 0.09 mg/L clethodim and 0.18 mg/L fluazifop-P were chosen as discriminant based on rate responses of each biotype to increasing herbicide dose. At 5 d after treatment (DAT), the amounts of clethodim required to reduce coleoptile length by 50% (GR50) for the R and S seedlings were 462.5 and 24.8 mg/L, respectively, resulting in an R:S ratio of 18.7. The fluazifop GR50 values for the R and S seedlings were 618.7 and 17.5 mg/L, respectively, resulting in a R:S ratio of 35.4.

Reports of resistance to grass-selective herbicides, including johnsongrass (Sorghum halepense) resistant to fluazifop-P, have become quite common. Experiments were conducted to determine if fluazifop-P resistance could be transferred from johnsongrass to crop sorghum (Sorghum bicolor) and to identify the heritability of resistance in the progeny. A population of male sterile, fluazifop-P–sensitive sorghum, AKS-82, was interplanted with fluazifop-P–resistant johnsongrass and progeny treated with 0.105 kg ai/ha fluazifop-P postemergence (POST). Surviving seedlings were backcrossed to fluazifop-P–resistant johnsongrass. Viable plants from this successful cross were then testcrossed to another sensitive sorghum, TX622. These testcross progeny were then screened for herbicide resistance by again applying fluazifop-P POST at 0.105 kg /ha. Chi-square analysis revealed that resistance to fluazifop-P was inherited by a single, dominant gene. Natural hybridization of johnsongrass and sorghum is possible, and transfer of herbicide resistance between species can occur.

Diagnosing herbicide-resistant weeds as a first step in resistance management and monitoring their nature, distribution, and abundance demands efficient and effective screening tests. This review summarizes and recommends appropriate seed sampling techniques, protocols for screening weeds for resistance to herbicides of different sites of action, interpretation of results, and information given to the grower. Elements common to all screening procedures are reviewed. Choosing appropriate discriminating doses to distinguish between resistant and susceptible weed biotypes is the most important factor in achieving accurate and consistent results. Interpretation of results is also critical because resistant weeds may comprise a small portion of the population in suspected accessions or biotypes.