Lack of S-adenosylmethionine Results in a Cell Division Defect in Escherichia Coli

Overview

Journal J Bacteriol

Publisher American Society for Microbiology

Specialty Microbiology

Date 1998 Jul 11

PMID 9658005

Citations 20

Authors

E B Newman

L I Budman

E C Chan

R C GREENE

R T Lin

C L Woldringh

R Dari

Affiliations

Soon will be listed here.

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.

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