PMID:9658005
| Citation |
Newman, EB, Budman, LI, Chan, EC, Greene, RC, Lin, RT, Woldringh, CL and D'Ari, R (1998) Lack of S-adenosylmethionine results in a cell division defect in Escherichia coli. J. Bacteriol. 180:3614-9 |
|---|---|
| Abstract |
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. |
| Links | |
| Keywords |
Bacterial Proteins/drug effects; Bacterial Proteins/genetics; Bacterial Proteins/metabolism; Cell Division/drug effects; Cell Division/physiology; DNA Methylation; DNA-Binding Proteins/metabolism; DNA-Binding Proteins/pharmacology; Escherichia coli/enzymology; Escherichia coli/growth & development; Escherichia coli/metabolism; Escherichia coli Proteins; Leucine/metabolism; Leucine/pharmacology; Leucine-Responsive Regulatory Protein; Methionine Adenosyltransferase/drug effects; Methionine Adenosyltransferase/metabolism; S-Adenosylmethionine/deficiency; S-Adenosylmethionine/genetics; Transcription Factors |
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