A kochia (Kochia scoparia) biotype resistant to triazine and ALS-inhibiting herbicides

A kochia biotype from McDonough County Illinois, was suspected to be resistant to both triazine and acetolactate synthase (ALS)-inhibiting herbicides. We performed greenhouse and laboratory experiments to confirm, quantify, and determine the molecular basis of multiple herbicide resistance in this biotype. Whole-plant phytotoxicity assays confirmed that the biotype was resistant to triazine (atrazine), imidazolinone (imazethapyr), and sulfonylurea (thifensulfuron and chlorsulfuron) herbicides. Relative to a susceptible kochia biotype, resistance to these herbicides ranged from 500- to > 28,000-fold. The kochia biotype from McDonough County also displayed high levels of resistance (2,000- to 3,000-fold) to ALS-inhibiting herbicides in in vivo ALS enzyme assays, indicating that resistance to these herbicides was site-of-action mediated. Results from chlorophyll fluorescence assays indicated that triazine resistance was also site-of-action mediated. Foliar applications of atrazine had little or no effect on photosynthesis in the resistant biotype, even when atrazine concentrations were 10(8)-fold higher than needed to inhibit photosynthesis in the susceptible biotype. A region of the gene encoding the DI protein of photosystem II and all of the open reading frame of the gene encoding AL-S were sequenced and compared between the resistant and susceptible biotypes. Resistance to triazine and ALS-inhibiting herbicides in the kochia biotype From McDonough County was conferred by, respectively, a glycine for serine substitution at residue 264 of the DI protein and a leucine for tryptophan substitution at residue 570 of ALS.