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.
Nomenclature: Imazethapyr; eastern black nightshade, Solanum ptycanthum L. SOLPT.
