Field experiments were conducted during the winters of 1987–88 and 1988–89 at Haryana Agricultural University, Hisar, India to evaluate the response of winter wild oat to sowing date and isoproturon application time in wheat. In another experiment, the effect of sowing time on emergence and growth of winter wild oat and wheat sown separately was studied. The treatments that provided more than 75% control of winter wild oat were: isoproturon at 0.75 kg ha−1 applied at the 2-leaf stage of winter wild oat; isoproturon 1 kg ha−1 applied at the 4-leaf stage of winter wild oat in the November 30 planting; and isoproturon 0.50 kg ha−1 applied at the 1- to 2-leaf stage of winter wild oat in the December 20 sowing. Isoproturon did not provide more than 50% control of winter wild oat in the November 10 sowing. Mortality of winter wild oat increased from 38 to 72 to 87% in November 10, November 30, and December 20 sowings, respectively. Mortality of winter wild oat was similar in November 30 and December 20 sowings but higher grain yield was recorded in November 30 sowing. Due to vigorous growth of winter wild oat in the November 10 sowing, isoproturon did not provide good control. December 20 sowing favored wheat growth due to lower density and late emergence of winter wild oat but reduction in wheat grain yield was greater. When averaged over isoproturon treatments, the grain yield of wheat was 4607, 5297, and 4457 kg ha−1 in the November 10, November 30, and December 20 sowings, respectively.

Field experiments were conducted during the winters of 1986–87 and 1987–88 at Haryana Agricultural University, Hisar, India to classify the ability of winter wheat cultivars to compete with wild oat. Wild oat reduced winter wheat grain yield by 17 to 62% depending upon cultivar. WH-147 and HD-2285 were the most competitive cultivars. Winter wheat dry matter accumulation and grain yield were negatively correlated with wild oat dry matter. A high number of tillers, particularly in HD-2009, WH-291, and S-308, did not always translate into grain yield advantage in wild oat-infested plots. Wheat height and dry matter accumulation per unit area during early crop growth were better characters than number of tillers for predicting the competitive ability of wheat cultivars to wild oat.

Resistance to the methyl ester of diclofop, an aryloxyphenoxypropionate graminicide, was shown for a wild oat (Avena fatua) population from Western Australia, and marked resistance to a range of aryloxyphenoxypropionate and cyclohexanedione graminicides was detected in a winter wild oat (Avena sterilis ssp. ludoviciana) population from South Australia. The A. sterilis biotype exhibited high levels of resistance to the aryloxyphenoxypropionate herbicides diclofop, fluazifop, haloxyfop, fenoxaprop, quizalofop, propaquizafop, and quinfurop and low levels of resistance to the cyclohexanedione herbicides sethoxydim, tralkoxydim, and cycloxydim. Ratios of LD50 values for responses of resistant and susceptible A. sterilis to the aryloxyphenoxypropionate herbicides were between 20 for propaquizafop and > 1,000 for fluazifop, and were between 2.5 and 3 for the cyclohexanedione herbicides. The LD50 value for diclofop for the A. fatua biotype was 442 g ai ha-1 which was 2.7-fold that of a susceptible control. Thirty-three percent of the plants survived at the registered rate of application.

Aryloxyphenoxypropanoate (APP) herbicides, such as diclofop, depolarize membranes in parenchyma cells of coleoptiles and root tips, and isolated tonoplast or plasma membrane vesicles from a variety of plant species. Some APP-resistant biotypes of rigid ryegrass and wild oat repolarize membranes after removal of herbicide from a bathing medium. The repolarization ability does not require presence of either APP-insensitive acetyl coenzyme A carboxylase or an increased capacity for herbicide detoxification. The kinetics of depolarization and repolarization depend upon the herbicide, the herbicide concentration, the biotype, and the pH of the bathing solution. For rigid ryegrass, depolarization in the presence of diclofop acid is more rapid than in the presence of diclofop-methyl, and 50% depolarization required about 4 μM diclofop acid. Both the nonherbicidal S(–) and the herbicidal R(+) enantiomers of diclofop acid depolarized membranes in susceptible and resistant ryegrass. Susceptible biotypes regenerated transmembrane potentials following removal of the S(–) but not the R(+) enantiomer, whereas resistant biotypes repolarized following exposure to either enantiomer or a mixture of the two. The herbicide 2,4-D affected, in a complex manner, the ability of both susceptible and resistant ryegrass biotypes to depolarize and repolarize. It is postulated that the intracellular concentration of diclofop acid in susceptible and resistant plants is not the same due to differences in the partitioning of diclofop acid between the extracellular spaces and the cytoplasm. The mechanism producing the postulated difference is unknown, but observations on the proton extrusion capacity of both ryegrass and wild oats, the responses of ryegrass to [K+] and PCMBS, and the single-gene inheritance pattern of resistance in wild oats indicate that changes in the diclofop sensitivity of a plasma membrane protein involved in the generation of proton or ion gradients may be involved.