FIG 1.

Schematic representation of the major metabolic pathways of acetate metabolism. Acetate can be generated directly from pyruvate by decarboxylation (using the enzyme pyruvate oxidase, PoxB) or from acetyl-CoA via the intermediate acetyl-phosphate (Ac∼P) (reactions catalyzed by the enzymes phosphotransacetylase, Pta, and acetate kinase, AckA). Acetate can freely diffuse across the cell membrane in the protonated form (13), HAc, or as an acetate ion, Ac⁻, via the transporter ActP or SatP (38). Protons that enter the cell in the form of HAc can be expelled at the expense of energy. The enzyme acetyl-CoA synthetase, Acs, efficiently converts intracellular acetate into acetyl-CoA. Acetate is also involved in several metabolic pathways. For example, the biosynthesis of methionine is inhibited by acetate. Excess intracellular acetate perturbs the anion balance in the cell and thus could inhibit other metabolic reactions (20). The pool of the major intracellular anion, glutamate, is strongly reduced when the intracellular concentration of acetate is high.