Involvement of ack-pta operon products in α-ketobutyrate metabolism by Salmonella typhimurium

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Abstract
Summary The herbicide sulfometuron methyl inhibits acetolactate synthase II of Salmonella typhimurium, resulting in toxic accumulation of α-ketobutyrate. Four mutants, containing Tn10 insertions in the acetate kinase (ack) or phosphotransacetylase (pra) genes, were found among a collection of mutants hypersensitive to sulfometuron methyl. The genetic map location of these four Tn10 insertions at 46 min was indentical to that of ack and pta point mutants. The insertion and point mutants shared the following phenotypes: resistance to fluoroacetate, sensitivity to alizarin yellow, inability to utilize inositol as a sole carbon source, and hypersensitivity to sulfometuron methyl. Three of the four Tn10 insertion mutants were deficient in phosphotransacetylase but not in acetate kinase activities, indicating insertion of Tn10 in the pta gene. The fourth mutant contained an insertion in the ack gene and was deficient in both acetate kinase and phosphotransacetylase activities. This polarity is consistent with cotranscription of ack and pta. All ack and pta mutants tested were defective in α-ketobutyrate turnover. Acetate kinase and phosphotransacetylase are proposed to be part of a pathway for α-ketobutyrate metabolism. Propionyl-CoA, an intermediate of that pathway, and propionate, the product of the pathway, accumutated upon inhibition of acetolactate synthase.