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Originally published In Press as doi:10.1074/jbc.M600333200 on May 9, 2006

J. Biol. Chem., Vol. 281, Issue 29, 19822-19829, July 21, 2006
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Potassium/Proton Antiport System of Escherichia coli*

Martha V. Radchenko{ddagger}, Kimihiro Tanaka§, Rungaroon Waditee, Sawako Oshimi{ddagger}, Yasutomo Matsuzaki{ddagger}, Masahiro Fukuhara{ddagger}, Hiroshi Kobayashi||, Teruhiro Takabe, and Tatsunosuke Nakamura{ddagger}1

From the {ddagger}Department of Microbiology, Niigata University of Pharmacy and Applied Life Sciences, Niigata 950-2081, Japan, §Graduate School of Environmental and Human Sciences, Meijo University, Nagoya 468-8502, Japan, Research Institute of Meijo University, Tenpaku-ku, Nagoya, Aichi 468-8502, Japan, and ||Graduate School of Pharmaceutical Sciences, Chiba University, 1-8-1, Inohana, Chuo-ku, Chiba 260-8675, Japan

The intracellular level of potassium (K+) in Escherichia coli is regulated through multiple K+ transport systems. Recent data indicate that not all K+ extrusion system(s) have been identified (15). Here we report that the E. coli Na+ (Ca2+)/H+ antiporter ChaA functions as a K+ extrusion system. Cells expressing ChaA mediated K+ efflux against a K+ concentration gradient. E. coli strains lacking the chaA gene were unable to extrude K+ under conditions in which wild-type cells extruded K+. The K+/H+ antiporter activity of ChaA was detected by using inverted membrane vesicles produced using a French press. Physiological growth studies indicated that E. coli uses ChaA to discard excessive K+, which is toxic for these cells. These results suggest that ChaA K+/H+ antiporter activity enables E. coli to adapt to K+ salinity stress and to maintain K+ homeostasis.


Received for publication, January 12, 2006 , and in revised form, May 8, 2006.

* This work was supported by a grant-in-aid for scientific research from the Ministry of Education, Science, Sports, and Culture of Japan (14572051) and by a grant from the Promotion and Mutual Aid Corporation for Private Schools in Japan. 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.

1 To whom correspondence should be addressed: Dept. of Microbiology, Niigata University of Pharmacy and Applied Life Sciences, 5-13-2 Kamishin'ei-cho, Niigata 950-2081, Japan. Tel. and Fax: 81-25-268-1210; E-mail: tnak{at}niigata-pharm.ac.jp.


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