Summary Amaranthus hybridus L. populations (A, B and C) obtained from escapes in Massac County and Pope County fields in southern Illinois, USA were subjected to greenhouse and laboratory experiments to measure multiple resistance to triazine and acetolactate synthase (ALS)‐inhibiting herbicides and cross‐resistance between sulfonylurea and imidazolinone herbicides. Phytotoxicity responses of the three populations revealed that only population B exhibited multiple resistances to triazine and ALS‐inhibiting herbicides. This population was >167‐, >152‐ and >189‐fold resistant to atrazine, imazamox and thifensulfuron, respectively, at the whole plant level compared with the susceptible population. Population A was only resistant to triazines and population C was only resistant to ALS‐inhibiting herbicides. Results from in vivo ALS enzyme and chlorophyll fluorescence assays confirmed these findings and indicated that an altered site‐of‐action mediated resistance to both triazine and ALS‐inhibiting herbicides. Gene sequencing revealed that a glycine for serine substitution at residue 264 of the D1 protein, and a leucine for tryptophan substitution at residue 574 of ALS were the causes of resistance for the three populations.
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Maertens et al. (2004) studied this question.
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