A common sunflower population from Howard, SD (HSD) was previously determined to be cross-resistant to imazethapyr and chlorimuron-ethyl, both acetolactate synthase–inhibiting (ALS) herbicides. Experiments were conducted to determine if target-site polymorphisms could act as a mechanism of ALS-inhibitor herbicide resistance in the HSD common sunflower. Approximately 1,600 nucleotides were amplified by polymerase chain reaction and sequenced from putative ALS gene(s) in common sunflower and Jerusalem artichoke. In sunflower, two different amplification products were detected that differed by a nine-basepair deletion. This suggested the presence of at least two ALS genes in common sunflower that could contribute to the herbicide resistance phenotype. In addition, an Ala205 to Val205 substitution was observed in several clones from resistant common sunflower (amino acid position is relative to the full-length mouse-ear cress ALS protein). Previously documented mutations at this position in other species indicated that it might play a vital role in conferring resistance to one or more ALS-inhibitor herbicides.
Nomenclature: Chlorimuron-ethyl; imazethapyr; common sunflower, Helianthus annuus L. HELAN; Jerusalem artichoke, Helianthus tuberosus L. HELTU; mouse-ear cress, Arabidopsis thaliana (L.) Heynh. ARBTH.