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Journal of Bacteriology, July 2008, p. 4933-4940, Vol. 190, No. 14
0021-9193/08/$08.00+0     doi:10.1128/JB.00405-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

A Specialized Citric Acid Cycle Requiring Succinyl-Coenzyme A (CoA):Acetate CoA-Transferase (AarC) Confers Acetic Acid Resistance on the Acidophile Acetobacter aceti{triangledown} ,{dagger}

Elwood A. Mullins,1,2 Julie A. Francois,2 and T. Joseph Kappock1,2*

Department of Biochemistry, Purdue University, West Lafayette, Indiana 47907,1 Department of Chemistry, Washington University in St. Louis, St. Louis, Missouri 631302

Received 21 March 2008/ Accepted 14 May 2008

Microbes tailor macromolecules and metabolism to overcome specific environmental challenges. Acetic acid bacteria perform the aerobic oxidation of ethanol to acetic acid and are generally resistant to high levels of these two membrane-permeable poisons. The citric acid cycle (CAC) is linked to acetic acid resistance in Acetobacter aceti by several observations, among them the oxidation of acetate to CO2 by highly resistant acetic acid bacteria and the previously unexplained role of A. aceti citrate synthase (AarA) in acetic acid resistance at a low pH. Here we assign specific biochemical roles to the other components of the A. aceti strain 1023 aarABC region. AarC is succinyl-coenzyme A (CoA):acetate CoA-transferase, which replaces succinyl-CoA synthetase in a variant CAC. This new bypass appears to reduce metabolic demand for free CoA, reliance upon nucleotide pools, and the likely effect of variable cytoplasmic pH upon CAC flux. The putative aarB gene is reassigned to SixA, a known activator of CAC flux. Carbon overflow pathways are triggered in many bacteria during metabolic limitation, which typically leads to the production and diffusive loss of acetate. Since acetate overflow is not feasible for A. aceti, a CO2 loss strategy that allows acetic acid removal without substrate-level (de)phosphorylation may instead be employed. All three aar genes, therefore, support flux through a complete but unorthodox CAC that is needed to lower cytoplasmic acetate levels.

* Corresponding author. Mailing address: 175 S. University Street, West Lafayette, IN 47907-2063. Phone: (765) 494-8383. Fax: (765) 494-7897. E-mail: kappock{at}purdue.edu

{triangledown} Published ahead of print on 23 May 2008.

{dagger} Supplemental material for this article may be found at http://jb.asm.org/.

Journal of Bacteriology, July 2008, p. 4933-4940, Vol. 190, No. 14
0021-9193/08/$08.00+0     doi:10.1128/JB.00405-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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