‘Karla’, ‘Klages', ‘Morex’, and ‘Steptoe’ cultivars of spring barley (Hordeum vulgare L.) differed in susceptibility to postemergence recommended application rates of diclofop {(±)-2-[4-(2,4-dichlorophenoxy) phenoxy] propanoic acid}, difenzoquat [1,2-dimethyl-3,5-diphenyl-1H-pyrazolium], chlorsulfuron {2-chloro-N-[[(4-methoxy-6-methyl-1,3,5-triazin-2-yl)amino] carbonyl] benzenesulfonamide}, and metribuzin [4-amino-6-(1,1-dimethylethyl)-3-(methylthio)-1,2,4-triazin-5(4H)-one] in 1981 and 1982. Metribuzin injured Morex, and difenzoquat injured all cultivars within 2 weeks after herbicide application. Metribuzin reduced height and crop biomass compared to the hand-weeded control. Herbicide treatments did not affect grain yield at Moscow, ID, in either year. However, metribuzin reduced yield of Karla and Morex, and diclofop reduced yield of Karla compared to the hand-weeded control at Pullman, WA, in 1982. Barley injury and grain yield loss depended on herbicide treatment and cultivar. Early season herbicide injury to barley did not indicate grain yield response at harvest.

A seedling bioassay was used to determine the response of triallate-resistant (R) and -susceptible (S) wild oat populations to difenzoquat and EPTC. The bioassay, based on seedling shoot length at 10 d after treatment, provided a reliable and rapid means of determining if wild oat populations were resistant to difenzoquat. Using a bioassay concentration of 15 ppm difenzoquat, it was possible to identify populations that were resistant to the recommended foliar-applied rate (0.85 kg ai/ha). Expected herbicide dosages that reduced shoot length by 50% (ED50) derived from nonlinear regression analysis indicated three and two levels of response to difenzoquat among eight S and seven R populations, respectively, indicating within population variability in their response to difenzoquat. Of the populations tested, none was resistant to EPTC. On the contrary, some R populations had lower ED50 values than did S populations, suggesting an increased sensitivity to EPTC.

Field studies were conducted in Saskatchewan to evaluate the effect of herbicides on annual canarygrass (Phalaris canariensis L.) and associated weeds. Bromoxynil (3,5-dibromo-4-hydroxybenzonitrile) at 0.35 kg ai/ha, tank mixes of bromoxynil at 0.28 kg/ha plus the ester of MCPA [(4-chloro-2-methylphenoxy)acetic acid] at 0.28 kg ae/ha, linuron [N′-(3,4-dichlorophenyl)-N-methoxy-N-methylurea] at 0.28 kg ai/ha plus MCPA amine at 0.56 kg/ha, or propanil [N-(3,4-dichlorophenyI)propanamide] at 1.0 kg ai/ha plus MCPA ester at 0.28 kg/ha resulted in annual canarygrass seed and dry matter yields equal to the unsprayed check and excellent wild mustard (Sinapis arvensis L. # SINAR) and cow cockle (Vaccaria pyramidata Medik. # VAAPY) control. Metribuzin [4-amino-6-(1,1-dimethylethyl)-3-(methylthio)-1,2,4-triazin-5(4H)-one] at 0.21 kg ai/ha plus MCPA amine at 0.56 kg/ha reduced the crop stand in 1 out of 5 yr and seed yield every year. Postemergence application of difenzoquat (1,2-dimethyl-3,5-dipheny1-1H-pyrazolium) at 0.84 kg ai/ha or flamprop [N-benzoyl-N-(3-chloro-4-fluorophenyl)-DL-alanine] at 0.53 kg ai/ha, or preplant-incorporated triallate [S-(2,3,3-trichloro-2-propenyl)bis(1-methylethyl)carbamothioate] at 1.40 kg ai/ha optimized wild oat (Avena fatua L. # AVEFA) control with seed yields. Diclofop {(±)-2-[4-(2,4-dichlorophenoxy)phenoxy)propanoic acid} at 0.70 kg ai/ha severely damaged annual canarygrass in all years. Triallate applied at 1.40 kg/ha preplant or preemergence incorporated marginally reduced the crop stand and seed yield compared to the untreated controls in tolerance tests.

The effect of barley seeding rate and row spacing, and triallate, diclofop, and difenzoquat herbicide rate on barley grain yield and quality, and wild oat control were evaluated in field experiments near Bonners Ferry, Idaho, in 1989 and 1990. The purpose of the study was to develop integrated control strategies for wild oat in spring barley. Barley row spacing (9 and 18 cm) did not affect barley grain yield. Barley grain yield was greatest when barley was seeded at 134 or 201 kg ha–1 compared to 67 kg ha–1. Wild oat control increased as wild oat herbicide rate increased and barley grain yield was greatest when wild oat herbicides were applied. However, barley grain yield was similar when wild oat biomass was reduced by either 65 or 85% by applications of half and full herbicide rates, respectively. Net return was greatest when the half rate of herbicide was applied to 100 wild oat plants per m2 and was greatest when half or full herbicide rates were applied to 290 wild oat plants per m2. Net return increased when the seeding rate was increased to 134 or 201 kg ha–1 when no herbicide was applied and when 290 wild oat plants per m2 were present.

Rates and application timings of postemergence herbicides for wild oat control in spring wheat and barley were evaluated at Crookston, MN, from 1994 to 1996. Diclofop, imazamethabenz, and fenoxaprop plus MCPA plus thifensulfuron plus tribenuron were applied to one- to three-leaf wild oat; and difenzoquat, imazamethabenz, fenoxaprop plus MCPA plus thifensulfuron plus tribenuron, and fenoxaprop plus 2,4-D plus MCPA were applied to four- to five-leaf wild oat at 1/2 ×, 3/4 ×, and 1 × rates. Wild oat response to herbicide rate and timing was similar in wheat and barley. Wild oat control with 1/2 × rates generally was less than that with 3/4 × rates, which was lower than or similar to that with 1 × rates. Wild oat biomass was often reduced less with 1/2 × rates than 1 × rates. However, reducing herbicide rates generally did not influence grain yields or net economic return. Grain yields and net economic return were generally greater in herbicide-treated plots than in the nontreated control.

Response of wild oat (Avena fatua L.) at the three-leaf stage to five postemergence herbicides, asulam (methyl sulfanilylcarbamate), barban (4-chloro-2-butynyl m-chlorocarbanilate), diclofop {2-[4-(2,4-dichlorophenoxy)phenoxy] propanoic acid}, difenzoquat (1,2-dimethyl-3,5-diphenyl-1 H-pyrazolium), and flamprop [N-benzoyl-N-(3-chloro-4-fluorophenyl)-DL-alanine] was measured and compared in nine physiological and biochemical processes (chlorophyll content, photosynthesis, photosynthate translocation, and changes in ATP, lipids, DNA, RNA, amino acids, and proteins). Content of chlorophyll a and b was reduced by the application of diclofop and difenzoquat. Photosynthesis was inhibited with all five herbicides, but photosynthate translocation from the leaves to the roots was reduced only with diclofop, difenzoquat, and flamprop. ATP production was inhibited by all herbicides except flamprop, which increased the ATP content. Incorporation of 32P into lipids was reduced by all herbicides except asulam. The incorporation of 32P into nucleic acids (DNA and RNA) was inhibited by all five herbicides. Serine and threonine, especially the latter, accumulated in large quantity with all herbicides except difenzoquat. Protein content (water-soluble,-insoluble, and total amount) was reduced by asulam, diclofop, and flamprop, but barban and difenzoquat reduced water-insoluble and total proteins only. Apparently, all herbicides examined affected more than one physiological function and biochemical process in wild oat.

Experiments were conducted in each of two seasons to determine possible effects of diclofop, difenzoquat, dinoseb, and mecoprop on the incidence of take-all disease and grain yield of winter wheat. All of the herbicides, especially mecoprop, reduced incidence of take-all. Treatments increased grain yields the first year but not the second, compared to the inoculated weed-free control. None of the herbicides tested increased incidence or severity of take-all disease in either of the two seasons. The technique of inoculating disease-free soil was successful in obtaining uniform and reproducible incidence of disease.

Wild oat (Avena fatua L. ♯3 AVEFA) and Avena sterilis L. ♯ AVEST accessions from the United States were screened for tolerance to diallate [S-(2,3-dichloroallyl) diisopropylthiocarbamate], triallate [S-(2,3,3-trichloroallyl) diisopropylthiocarbamate], barban (4-chloro-2-butynyl m-chlorocarbanilate), diclofop {2-[4-(2,4-dichlorophenoxy) phenoxy] propanoic acid}, difenzoquat (1,2-dimethyl-3,5-diphenyl-1H-pyrazolium), flamprop [N-benzoyl-N-(3-chloro-4-fluorophenyl)-DL-alanine], and MSMA (monosodium methanearsonate). Some accessions were tolerant to more than one herbicide but none were tolerant to all herbicides. Tolerance to a herbicide was not restricted to certain areas of origin of the accessions, and tolerant accessions occurred even in locations that had not been treated previously with the herbicide. In general, accessions from Southern California and Arizona were shorter, produced more tillers, and required the least number of days to panicle emergence. However, accessions from within individual areas were nearly as variable in these characteristics as the entire 1200 accessions. Tolerance of accessions to flamprop, difenzoquat, MSMA, and diclofop was not due to low leaf surface area, since the tolerant accessions usually had the most leaf surface area. All the accessions tolerant to difenzoquat, MSMA, and flamprop, and three of the four accessions tolerant to diclofop, tillered less than the susceptible accessions.

Field experiments were conducted for 2 yr to determine the influence of picloram (4-amino-3,5,6-trichloropicolinic acid) and a commercial mixture of picloram plus 2,4-D [(2,4-dichlorophenoxy)acetic acid] (1:16, w/w) on control of wild oats (Avena fatua L. # AVEFA) with four postemergence herbicides. The phytotoxicity to wild oats of barban (4-chloro-2-butynyl m-chlorocarbanilate) or difenzoquat (1,2-dimethyl-3,5-diphenyl-1H-pyrazolium) in 1981 and diclofop {2-[4-(2,4-dichlorophenoxy)-phenoxy] propanoic acid} or flamprop [N-benzoyl-N-(3-chloro-4-fluorophenyl)-DL-alanine] in 1981 and 1982 was reduced when these herbicides were applied in a mixture with picloram plus 2,4-D. Consequently, the use of these mixtures for broad-spectrum weed control in one spray operation is not recommended. Picloram applied at a rate equivalent to the amount present in the picloram plus 2,4-D mixture did not influence the control of wild oats obtained with any herbicide, indicating that the antagonism was due to the 2,4-D component of the picloram plus 2,4-D mixture.

The diversity of resistance among wild oat collected before and after commercial introduction of imazamethabenz, difenzoquat, diclofop, fenoxaprop-P, sethoxydim, and tralkoxydim was evaluated. Wild oat sampled in 1964 and 2000 from the Red River Valley of Minnesota and North Dakota were screened for resistance. Nearly 43% of the 1964 collections were susceptible (S) to all six herbicides, whereas only 9% were S by 2000. The frequency of resistance in 2000 compared with 1964 increased for all six herbicides, and 27 phenotype response groups to the six herbicides occurred in 2000 vs. 14 phenotype response groups for the 1964 collection. The proportion of resistant (R) plants increased faster for the aryloxyphenoxypropionate (APP) herbicides, diclofop and fenoxaprop-P, than for the cyclohexanedione (CHD) herbicides, sethoxydim and tralkoxydim. High diversity of resistance responses was observed in wild oat to acetyl-coenzyme A carboxylase–inhibitor herbicides, suggesting that there may be multiple APP herbicide– or CHD herbicide–specific resistance mechanisms in addition to those that confer cross-resistance. The trend of resistance response generally indicates that increased exposure to herbicides in wild oat may confer resistance to newly introduced but unrelated herbicides.

Eight hard red spring wheat cultivars were tested for tolerance to five postemergence grass herbicides at two locations in Minnesota in 1999 and 2000 at the labeled, one and one-half, or twice the labeled rate. Fenoxaprop plus safener and ICIA 0604 caused the least injury and did not reduce grain yield for most cultivars. Flucarbazone caused intermediate injury and a slight decrease in grain yield for half the cultivars tested. Difenzoquat caused the most injury, regardless of whether the cultivar was genetically sensitive to difenzoquat. Tank-mixing difenzoquat with imazamethabenz reduced injury, even for cultivars that were not genetically sensitive to difenzoquat. Drought stress before application of the postemergence grass herbicides that contain difenzoquat resulted in more potential for crop injury. Excess precipitation combined with high temperatures after application resulted in more potential for crop injury for the other postemergence grass herbicides included in this experiment.

A bioassay, based on seedling shoot inhibition with difenzoquat at 10 mg/L, provides a rapid means of predicting hard red spring wheat (HRSW) cultivar response to foliar-applied difenzoquat. The tolerance of several cultivars to difenzoquat was determined by shoot length inhibition in the laboratory, and by visible crop injury and shoot dry weight in the greenhouse. Of the 19 cultivars tested, one cultivar that was susceptible in the laboratory assay was intermediate in tolerance to difenzoquat in the greenhouse assay; two cultivars that were tolerant in the laboratory bioassay were of intermediate tolerance in the greenhouse assay. Results from laboratory and greenhouse studies both identified cultivars distinctly susceptible to difenzoquat. Shoot inhibition indicated that HRSW cultivar susceptibility to difenzoquat involves continuous variation from tolerant to susceptible. This may explain why some cultivars show differential responses to difenzoquat under different environmental conditions.