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J Bacteriol, July 1998, p. 3614-3619, Vol. 180, No. 14
0021-9193/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Lack of S-Adenosylmethionine Results in a Cell Division Defect in Escherichia coli

E. B. Newman,1,* L. I. Budman,1 E. C. Chan,2 R. C. Greene,3 R. T. Lin,4 C. L. Woldringh,5 and R. D'Ari6

Biology Department, Concordia University Montreal, Quebec H3G 1M8,1 Microbiology Department, Faculty of Medicine, McGill University, Montreal, Quebec H3A 2B4,2 and Lady Davis Institute for Medical Research, Montreal, Quebec H3T 1E2,4 Canada; U.S. Veterans' Administration Medical Center and Department of Biochemistry, Duke University Medical Center, Durham, North Carolina 277103; Institute for Molecular Cell Biology, Section Molecular Cytology, BioCentrum, University of Amsterdam, 1098 SM Amsterdam, The Netherlands5; and Institut Jacques Monod (CNRS, Université Paris 7, Université Paris 6), F-75251 Paris, Cedex 05, France6

Received 31 March 1998/Accepted 19 May 1998

The enzyme S-adenosylmethionine (SAM) synthetase, the Escherichia coli metK gene product, produces SAM, the cell's major methyl donor. We show here that SAM synthetase activity is induced by leucine and repressed by Lrp, the leucine-responsive regulatory protein. When SAM synthetase activity falls below a certain critical threshold, the cells produce long filaments with regularly distributed nucleoids. Expression of a plasmid-carried metK gene prevents filamentation and restores normal growth to the metK mutant. This indicates that lack of SAM results in a division defect.

* Corresponding author. Mailing address: Biology Department, Concordia University, 1455 de Maisonneuve Ave., Montreal, Quebec H3G 1M8, Canada. Phone: (514) 848-3410. Fax: (514) 848-2881. E-mail: Neweb{at}Vax2.Concordia.Ca.

J Bacteriol, July 1998, p. 3614-3619, Vol. 180, No. 14
0021-9193/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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