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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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