Populations of Setaria faberi and Digitaria sanguinalis cross-resistant to sethoxydim and fluazifop-P-butyl were identified in a vegetable cropping system in Wisconsin, USA, in 1991 and 1992 respectively. Experiments were conducted with partially purified acetyl-CoA carboxylase (ACCase) to determine whether resistance to sethoxydim and other ACCase inhibitors in S. faberi and D. sanguinalis resulted from altered enzyme activity. Based on I 50 values (the herbicide dose that inhibited ACCase activity by 50% compared with untreated ACCase), ACCase of the resistant accession of S. faberi was 4.8-, 10.6-and 319-fold resistant to clethodim, fluazifop-P acid and sethoxydim, respectively, compared with that of the susceptible accession. Similarly, ACCase of the resistant accession of D. sanguinalis was 5.8-, 10.3and 66-fold resistant to clethodim, fluazifop-P acid and sethoxydim respectively. These results indicated that resistance to ACCase inhibitors in these accessions of S. faberi and D. sanguinalis resulted from an altered ACCase enzyme that confers a very high level of resistance to sethoxydim.

Gene flow via pollen and inheritance of acetyl-coenzyme A carboxylase (ACCase) inhibitor resistance in giant foxtail have not been previously characterized. Therefore, experiments were conducted to quantify outcrossing rates and flowering periods of giant foxtail accessions resistant or susceptible to ACCase inhibitors and to determine the inheritance pattern of gene(s) that confer resistance. In greenhouse experiments, outcrossing rates between resistant and susceptible parents ranged from 0.24 to 0.73%, as gauged by the response of F1 plants to fluazifop-P. Resistant plants and susceptible plants flowered at similar times, with peak flowering occurring 63 to 67 d after planting. During this period, flower initiation was nearly twice as great for resistant plants as for susceptible plants. In inheritance experiments F2 plants segregated in a 1:2:1 ratio of resistant–intermediate–susceptible phenotypes after exposure to fluazifop-P, indicating that resistance was associated with a single nuclear, incompletely dominant allele. The very low rates of outcrossing among giant foxtail plants in the greenhouse indicate that gene flow of resistance traits in the field is likely to occur primarily by seed immigration rather than by pollen movement. However, gene flow of herbicide resistance traits via pollen provides a mechanism in which multiple resistance may develop among giant foxtail populations that are resistant to other classes of herbicides.

Solanum ptycanthum plants putatively resistant to acetolactate synthase (ALS) inhibitors were identified in a Wisconsin Glycine max field in 1999. Three- to four-leaf-stage S. ptycanthum plants in the greenhouse were 150, 120, and 5.9-fold resistant to imazethapyr, imazamox, and primisulfuron, respectively, compared with susceptible plants. In vivo ALS was 170- and less than 20-fold more resistant to imazethapyr and primisulfuron, respectively. These results suggested that the S. ptycanthum accession was highly resistant to imazethapyr and imazamox, and that resistance was associated with insensitive ALS. This is the first confirmed occurrence worldwide of S. ptycanthum resistance to ALS inhibitors.

Giant foxtail putatively resistant to acetolactate synthase (ALS) inhibitors has been reported widely in the upper Midwest, typically in fields with a history of ALS inhibitor use in continuous corn or corn–soybean rotation. However, it is not known whether these giant foxtail populations vary in their response to ALS inhibitors. Therefore, our objectives were to confirm and quantify resistance of giant foxtail accessions from Wisconsin, Minnesota, and Illinois to imidazolinone and sulfonylurea herbicides; to determine the mechanism of resistance; and to determine the mechanism of resistance inheritance. Dose–response experiments using three- to four-leaf stage giant foxtail plants in the greenhouse confirmed cross-resistance of the Wisconsin, Minnesota, and Illinois accessions to imazethapyr and nicosulfuron. Based on ED50 values (the effective dose that reduced shoot dry biomass by 50% compared to the nontreated plants), the Wisconsin, Minnesota, and Illinois accessions were 16-, 17-, and 15-fold resistant to imazethapyr, respectively, and 21-, 19-, and 9-fold resistant to nicosulfuron, respectively, compared to susceptible accessions. In contrast, all accessions were susceptible and responded similarly to fluazifop-P. Based on an in vivo ALS assay, the Wisconsin, Minnesota, and Illinois accessions were > 750-, > 320-, and > 670-fold resistant to imazethapyr, respectively, and 1,900-, > 1,900-, and 80-fold resistant to nicosulfuron, respectively, compared to susceptible accessions. To determine the inheritance of resistance traits, hybrid F1 families were generated from crosses between ALS inhibitor–susceptible and -resistant plants from Minnesota. Three distinct plant phenotypes—resistant (R), intermediate (I), and susceptible (S)—were identified in the F2 generation following exposure to imazethapyr. In repeated experiments, these phenotypes segregated in a 1:2:1 (R:I:S) ratio, indicative of a trait associated with a single, nuclear, semidominant allele.

Experiments were conducted to determine the inheritance of resistance in a Wisconsin accession of eastern black nightshade to acetolactate synthase (ALS) inhibitors. ALS-inhibitor–susceptible (S) and ALS-inhibitor–resistant (R) plants were crossed (S × R), and inheritance was characterized in F1 and F2 generations. Inheritance was characterized further in progeny of reciprocal crosses (R × S) and backcrosses (BCs) (S × F1 and R × F1). In dose–response experiments, three- to four-leaved F1 plants were intermediate in response to imazethapyr compared with parent R and S plants. The imazethapyr ED50 value (the effective dose that reduced shoot dry biomass by 50% compared with nontreated plants) was 99.6 ± 13.6, 32.5 ± 8.9, 24.5 ± 3.3, and 0.6 ± 0.1 g ae ha−1 for R, F1 (R × S), F1 (S × R), and S plants, respectively. Similarly, the response of in vivo ALS activity in F1 plants to imazethapyr was intermediate compared with that of parent R and S plants. To differentiate among phenotypes in F2 generations and in BC generations, the response of three- to four-leaved plants to imazethapyr applied in a single dose was scored 21 d after treatment as R (no imazethapyr symptomology), S (total plant necrosis), or intermediate (I, severely stunted plants with chlorotic and twisted leaves at the apical meristem). R, I, and S phenotypes segregated in a 1:2:1 ratio in the F2 generation. S and I phenotypes segregated in a 1:1 ratio in progeny from F1 BCs to the S parent. Similarly, R and I phenotypes segregated in a 1:1 ratio in progeny from BCs to the R parent. Eastern black nightshade resistance to ALS inhibitors is associated with a single, nuclear, incompletely dominant allele, which codes for an insensitive form of the target ALS enzyme.