Previous research revealed that resistance to cloransulam in at least one population of common ragweed was conferred by an altered herbicide target site, specifically, by a tryptophan-to-leucine amino acid substitution at position 574 (W574L) of acetolactate synthase (ALS). In this study, 22 common ragweed populations, several of which were suspected cloransulam resistant, were assayed to determine if the W574L ALS substitution was correlated with resistance to ALS inhibitors. From each population, 16 greenhouse-grown plants were treated with cloransulam, and another 16 were treated with imazamox. Plant dry weights were recorded 20 d after treatment and individual plants were considered resistant if their dry weight exceeded 50% of that of nonherbicide-treated controls. For each herbicide-treated plant, allele-specific primers were used in polymerase chain reactions to determine whether the ALS alleles contained leucine or tryptophan codons at position 574. Of the 352 plants treated with cloransulam, 70 were determined to be resistant, and all but two contained one or more Leu574 alleles. The frequency of imazamox resistance was much higher than that of cloransulam in the populations, with 149 of 352 plants identified as imazamox resistant. However, only about half (80) of the imazamox-resistant plants contained one or more Leu574 alleles. Correlation of imazamox resistance and Leu574 alleles was population dependent. ALS activity assays confirmed that imazamox resistance in plants from at least one population was due to an altered target site, even though plants from that population did not have a W574L substitution. These results lead to the conclusion that a Leu574 allele is the predominant basis for cloransulam resistance in common ragweed; however, other mechanisms of resistance to ALS inhibitors exist in some populations.

Overuse of acetolactate synthase (ALS)–inhibiting herbicides in rice has ledto the evolution of halosulfuron-resistant rice flatsedge in Arkansas andMississippi. Resistant accessions were cross-resistant to labeled fieldrates of ALS-inhibiting herbicides from four different families, incomparison to a susceptible (SUS) biotype. Resistance index of Arkansas andMississippi accessions based on an R/S ratio of the lethal dose required for50% plant mortality (LD50) to bispyribac-sodium, halosulfuron,imazamox, and penoxsulam was ≥ 21-fold. Control of Arkansas, Mississippi,and SUS accessions with labeled field rates of 2,4-D, bentazon, and propanilwas ≥ 93%. An enzyme assay revealed that an R/S ratio for 50% inhibition (I50) of ALS for halosulfuron was 2,600 and 200 in Arkansasand Mississippi, respectively. Malathion studies did not reveal enhancedherbicide metabolism in resistant plants. The ALS enzyme assay andcross-resistance studies point toward altered a target site as the potentialmechanism of resistance. Trp574–Leu amino acid substitutionwithin the ALS gene was found in both Arkansas andMississippi rice flatsedge accessions using the Illumina HiSeq platform,which corresponds to the mechanism of resistance found in many weed species.Field-rate applications of 2,4-D, bentazon, and propanil can be used tocontrol these ALS-resistant rice flatsedge accessions.