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Journal of Bacteriology, September 2004, p. 6032-6041, Vol. 186, No. 18
0021-9193/04/$08.00+0     DOI: 10.1128/JB.186.18.6032-6041.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Escherichia coli Glutamate- and Arginine-Dependent Acid Resistance Systems Increase Internal pH and Reverse Transmembrane Potential

Hope Richard and John W. Foster*

Department of Microbiology and Immunology, University of South Alabama College of Medicine, Mobile, Alabama

Received 20 February 2004/ Accepted 22 June 2004

Due to the acidic nature of the stomach, enteric organisms must withstand extreme acid stress for colonization and pathogenesis. Escherichia coli contains several acid resistance systems that protect cells to pH 2. One acid resistance system, acid resistance system 2 (AR2), requires extracellular glutamate, while another (AR3) requires extracellular arginine. Little is known about how these systems protect cells from acid stress. AR2 and AR3 are thought to consume intracellular protons through amino acid decarboxylation. Antiport mechanisms then exchange decarboxylation products for new amino acid substrates. This form of proton consumption could maintain an internal pH (pHi) conducive to cell survival. The model was tested by estimating the pHi and transmembrane potential ({Delta}{Psi}) of cells acid stressed at pH 2.5. During acid challenge, glutamate- and arginine-dependent systems elevated pHi from 3.6 to 4.2 and 4.7, respectively. However, when pHi was manipulated to 4.0 in the presence or absence of glutamate, only cultures challenged in the presence of glutamate survived, indicating that a physiological parameter aside from pHi was also important. Measurements of {Delta}{Psi} indicated that amino acid-dependent acid resistance systems help convert membrane potential from an inside negative to inside positive charge, an established acidophile strategy used to survive extreme acidic environments. Thus, reversing {Delta}{Psi} may be a more important acid resistance strategy than maintaining a specific pHi value.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, University of South Alabama College of Medicine, 307 University Blvd., Mobile, AL 36688. Phone: (251) 460-6323. Fax: (251) 460-7931. E-mail: fosterj{at}sungcg.usouthal.edu.

Journal of Bacteriology, September 2004, p. 6032-6041, Vol. 186, No. 18
0021-9193/04/$08.00+0     DOI: 10.1128/JB.186.18.6032-6041.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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