Kochia growing on an industrial site where chlorsulfuron was applied repeatedly over several seasons was confirmed to be resistant to chlorsulfuron and several other acetolactate synthase (ALS) -inhibiting herbicides. In growth room experiments, resistant (R) plants were 2 to >180 times more resistant to five sulfonylurea herbicides and one imidazolinone herbicide (imazethapyr) than susceptible (S) plants, as measured by the ratio of dosages required to inhibit shoot dry matter accumulation by 50% (GR50 R/S). Similarly, in vitro assays of ALS activity indicated that from 3 to 30 times more herbicide was required to inhibit the enzyme from R plants than from S plants. Results of ALS enzyme assays indicated that R kochia was approximately equally resistant to metsulfuron, triasulfuron, and thifensulfuron, and 2.5 times more resistant to tribenuron than thifensulfuron. However, the response of R kochia growing in a spring wheat crop in the field was not consistent with results of the ALS enzyme assays. In field experiments, thifensulfuron at 32 g ai ha−1 had little effect on R kochia. In contrast, metsulfuron, triasulfuron, and tribenuron at 8 g ha−1 did not reduce R kochia seedling densities, but caused severe stunting such that 2 mo after treatment the shoot biomass of plants in untreated plots was four times greater than in sprayed plots. Herbicides with alternative modes of action including fluroxypyr, bromoxynil/MCPA ester, dichlorprop/2,4-D ester, and 2,4-D ester provided good control of R kochia in the field. Quinclorac did not reduce kochia densities, but surviving plants were stunted. To delay or avoid development of ALS inhibitor-resistant kochia populations, these alternative herbicides applied alone or in tank mixtures could be incorporated into a herbicide rotation.

Ten corn inbred lines were field evaluated for their tolerance to DPX-M6316 at 32 and 64 g ai/ha. Inbreds ‘A619′, ‘A641′, and ‘ND246’ were highly susceptible to DPX-M6316; inbreds ‘A671′, ‘A632′, and ‘B73’ were highly tolerant; and inbreds ‘A654′, ‘CM105′, ‘W153R’, and ‘M017’ were intermediate in their response. The basis for differential tolerance was studied by comparing the susceptibility of acetolactate synthase (ALS) to inhibition by DPX-M6316 in tolerant A671 and susceptible A619, and by examining the absorption, translocation, and metabolism of DPX-M6316 in both genotypes. I50 values for DPX-M6316 inhibition of ALS activity in extracts from etiolated shoots of A671 and A619 were similar, 15.6 and 17.4 nM, respectively. There was little difference in 14C-DPX-M6316 absorption by the two inbreds, but twice as much of the absorbed 14C was translocated out of the treated leaf of A619 (13%) compared to A671 (6%). Differences in translocation may have been due to much more rapid DPX-M6316 metabolism in A671 than in A619. Extracts from treated leaves of A671 had only 23% DPX-M6316 remaining 5.5 h after treatment (HAT) compared to 78% DPX-M6316 remaining in extracts from A619 leaves. Therefore, rate of metabolism was the major factor involved in the tolerance of A671 and the susceptibility of A619 to DPX-M6316.

Laboratory experiments were conducted to determine the physiological mechanism of tall morningglory resistance to the experimental cotton herbicide DPX-PE350. Tall morningglory, a resistant species, was compared with entireleaf morningglory, a sensitive species, to evaluate inhibition at the site of action, the acetolactate synthase (ALS) enzyme (E.C.4.1.3.18), by DPX-PE350 as well as uptake, translocation, and metabolism of DPX-PE350. No differences were found between species in the concentration required to inhibit the ALS enzyme by 50% (I50), or in uptake and translocation of the herbicide. Tall morningglory metabolized the herbicide more rapidly than did entireleaf morningglory. Tall morningglory contained 3.6 and 1.4 times more metabolites of DPX-PE350 than did entireleaf morningglory 6 and 24 h after treatment, respectively. Tall morningglory produced an O-desmethyl metabolite from the 3,5-dimethoxypyrimidine moiety of DPX PE350 that was not found in entireleaf morningglory. These data suggest that the ability of tall morningglory to more rapidly metabolize DPX-PE350, possibly through the production of the pyrimidinyldesmethyl metabolite, may be the mechanism of resistance to DPX-PE350.