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J. Biol. Chem., Vol. 278, Issue 25, 22846-22852, June 20, 2003

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Polyamines and Glutamate Decarboxylase-based Acid Resistance in Escherichia coli^*

Il Lae Jung and In Gyu Kim 

From the Department of Radiation Biology, Environmental Radiation Research Group, Korea Atomic Energy Research Institute, P. O. Box 105, Yusong, Taejon 305-600, Korea

The expression of gadA and gadB, which encode two glutamate decarboxylases (GADs) of Escherichia coli, is induced by an acidic environment and participate in acid resistance. In this study, we constructed a polyamine-deficient mutant and investigated the role of polyamines in acid resistance. The expression of gadA and gadB was shown to be dependent on polyamines. For that reason, the polyamine-deficient mutant was completely devoid of GAD activity and was very susceptible to low pH if large amounts of polyamines were not provided. We also showed that the polyamine-deficient mutant contained higher cAMP levels than the isogenic polyamine-proficient wild type, and cAMP negatively regulated the expression of gadA and gadB. Therefore, introduction of the cya (encoding adenylate cyclase) mutation allele into the polyamine-deficient mutant resulted in the increment of GAD activity and thus restored the reduced acid resistance of the mutant. The positive regulators, H-NS (histone-like protein, encoded by the hns gene) and RpoS (alternative RNA polymerase subunit, encoded by rpoS gene), also significantly governed the expression of gadA and gadB, respectively. However, polyamines did not regulate either the intracellular H-NS level or rpoS expression under these culture conditions. These results strongly suggest that there are at least two different regulatory systems in acid resistance, one is positive regulation via a H-NS/RpoS system and the other is negative regulation via a polyamine/cAMP system.

Received for publication, November 26, 2002

^* This work was supported by the Nuclear Research and Development Program from the Ministry of Science and Technology (MOST) of the Republic of Korea. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed: Dept. of Radiation Biology, Environmental Radiation Research Group, Korea Atomic Energy Research Inst., P. O. Box 105, Yusong, Taejon 305-600, Korea. Tel.: 82-42-868-8031; Fax: 82-42-861-9560; E-mail: igkim{at}kaeri.re.kr.

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