Weed Science · 2011 · 36 citations · 15 references
AgricultureGeneticsPlant SciencesHerbicide ResistancePlant GeneticsPlant Molecular BiologyAcetolactate Synthase InhibitionHerbicide Resistance MechanismsHerbicide ToleranceMolecular Basis Of ResistancePopulation Genetics In PlantsAcetolactate Synthase Inhibition ResistanceAcetolactate Synthase Inhibitor ResistanceAcetolactate Synthase MutationHerbicide Resistance GenesHerbicide Resistance GeneticsPopulation-level Resistance PatternsResistance-associated MutationsResistance-suppressing Mutations
The molecular basis of resistance to tribenuron-methyl, an acetolactate synthase (ALS)–inhibiting herbicide was investigated in four resistant (R) and three susceptible (S) flixweed populations. The resistance level in the R populations was assessed in whole-plant pot experiments in a greenhouse, and resistance indices ranged from 723 to 1422. The ALS genes of the three S populations and four R populations were cloned and sequenced, and the full coding sequence of the ALS gene of flixweed was 2,004 bp. The sequences of the ALS genes of the three S populations collected from Shaanxi, Gansu, and Tianjin were identical. Comparison of the ALS gene sequences of the S and R populations with Arabidopsis revealed that proline at position 197 of the ALS gene was substituted by leucine in R population SSX-2, by alanine in R population SSX-3, and by serine in R populations TJ-2 and GS-2. In another study of two R flixweed populations from Hebei and Shaanxi, resistance was also related to mutation at position 197 of the ALS gene. Both studies confirmed tribenuron-methyl resistance in flixweed in China, with the resistance mechanism being conferred by specific ALS point mutations at amino acid position 197.
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