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Journal of Bacteriology, January 2000, p. 371-376, Vol. 182, No. 2
0021-9193/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Viability of an Escherichia coli pgsA Null Mutant Lacking Detectable Phosphatidylglycerol and Cardiolipin

Shin Kikuchi, Isao Shibuya, and Kouji Matsumoto*

Department of Biochemistry and Molecular Biology, Faculty of Science, Saitama University, 255 Shimo-ohkubo, Urawa, Saitama 338-8570, Japan

Received 3 August 1999/Accepted 19 October 1999

Phosphatidylglycerol, the most abundant acidic phospholipid in Escherichia coli, has been considered to play specific roles in various cellular processes and is believed to be essential for cell viability. It is functionally replaced in some cases by cardiolipin, another abundant acidic phospholipid derived from phosphatidylglycerol. However, we now show that a null pgsA mutant is viable, if the major outer membrane lipoprotein is deficient. The pgsA gene normally encodes phosphatidylglycerophosphate synthase that catalyzes the committed step in the biosynthesis of these acidic phospholipids. In the mutant, the activity of this enzyme and both phosphatidylglycerol and cardiolipin were not detected (less than 0.01% of total phospholipid, both below the detection limit), although phosphatidic acid, an acidic biosynthetic precursor, accumulated (4.0%). Nonetheless, the null mutant grew almost normally in rich media. In low-osmolarity media and minimal media, however, it could not grow. It did not grow at temperatures over 40°C, explaining the previous inability to construct a null pgsA mutant (W. Xia and W. Dowhan, Proc. Natl. Acad. Sci. USA 92:783-787, 1995). Phosphatidylglycerol and cardiolipin are therefore nonessential for cell viability or basic life functions. This notion allows us to formulate a working model that defines the physiological functions of acidic phospholipids in E. coli and explains the suppressing effect of lipoprotein deficiency.

* Corresponding author. Mailing address: Department of Biochemistry and Molecular Biology, Faculty of Science, Saitama University, 255 Shimo-ohkubo, Urawa, Saitama 338-8570, Japan. Phone: 81-48-858-3406. Fax: 81-48-858-3698. E-mail: koumatsu{at}molbiol.saitama-u.ac.jp.

Journal of Bacteriology, January 2000, p. 371-376, Vol. 182, No. 2
0021-9193/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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