ilvB-encoded acetolactate synthase is resistant to the herbicide sulfometuron methyl.
The herbicide sulfometuron methyl is a potent inhibitor of the branched-chain amino acid biosynthetic enzyme acetolactate synthase (ALS) isolated from bacteria, fungi, and plants. However, it did not prevent growth of wild-type Salmonella typhimurium LT2 or Escherichia coli K-12. These species each contain two acetolactate synthase isozymes. Growth of S. typhimurium and E. coli mutants lacking ALS I was prevented by the herbicide, suggesting that activity of the remaining ALS isoenzyme (II or III, respectively) was stopped by sulfometuron methyl. Synthesis of ALS I requires either an relA function or an elevated cyclic AMP level. A relA mutant of S. typhimurium was inhibited by sulfometuron methyl on rich carbon sources that display a basal cyclic AMP level but not on poor carbon sources where the cyclic AMP concentration is elevated. When L-valine, which allosterically inhibits ALS I activity, was added, growth retardation of the relA- strain by sulfometuron methyl was observed on both poor and rich carbon sources. Enzymological analyses indicated that ALS I activities derived from both species were resistant to the herbicide. In contrast, activities of S. typhimurium ALS II and E. coli ALS III were abolished by sulfometuron methyl.
D000095:Acetolactate Synthase / Q000037:antagonists & inhibitors / Q000235:genetics*; D000483:Alleles; D000242:Cyclic AMP / Q000378:metabolism; D004926:Escherichia coli / Q000187:drug effects / Q000201:enzymology / Q000235:genetics*; D005796:Genes; D005798:Genes, Bacterial; D005838:Genotype; D007527:Isoenzymes / Q000235:genetics; D007700:Kinetics; D007652:Oxo-Acid-Lyases / Q000235:genetics*; D012486:Salmonella typhimurium / Q000187:drug effects / Q000235:genetics*; D013453:Sulfonylurea Compounds / Q000494:pharmacology*
D007527:Isoenzymes; D013453:Sulfonylurea Compounds; D000242:Cyclic AMP; D000095:Acetolactate Synthase; D007652:Oxo-Acid-Lyases; C042031:sulfometuron methyl