In 1996 a common sunflower population near Howard, SD, was suspected to be cross-resistant to imazethapyr and chlorimuron. Whole-plant acetolactate synthase (ALS) assays confirmed ALS-inhibitor resistance in the Howard biotype. The I₅₀ values (inhibition of 50% of the enzyme activity) indicated that the resistant population required 39 and 9 times more imazethapyr and chlorimuron, respectively, to obtain the same level of enzyme inhibition compared with the sensitive biotype. Herbicide dose response data supported the whole-plant enzyme assay data; control (> 90%) was not achieved with less than a four-times application rate of chlorimuron. Control with imazethapyr was not achieved even with a 16-times rate. Chlorimuron and imazethapyr controlled 70 and 95% of the population, respectively, when a four-times rate of each herbicide was applied separately. Differences in ¹⁴C-herbicide absorption were observed, suggesting that there may be physical or chemical differences in leaf surface composition between the resistant and sensitive biotypes. Although translocation of ¹⁴C-herbicide was less in the resistant biotype than in the sensitive biotype, the differences were not enough to explain chlorimuron and imazethapyr selectivity between the two biotypes. Overall results suggested that the differences in the common sunflower populations were attributed to an altered site of action on the ALS enzyme.

Nomenclature: Chlorimuron; imazethapyr; common sunflower, Helianthus annuus L. HELAN.