Previous Article | Next Article ![]()
Journal of Bacteriology, August 2000, p. 4437-4442, Vol. 182, No. 16
Department of Microbiology, University of
Sydney, Sydney, New South Wales 2006, Australia
Received 13 March 2000/Accepted 22 May 2000
Escherichia coli adapted to glucose-limited chemostats
contained mutations in ptsG resulting in V12G, V12F, and
G13C substitutions in glucose-specific enzyme II (EIIGlc)
and resulting in increased transport of glucose and
methyl-
0021-9193/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Substrate Specificity and Signal Transduction
Pathways in the Glucose-Specific Enzyme II (EIIGlc)
Component of the Escherichia coli Phosphotransferase
System
-glucoside. The mutations also resulted in faster growth on
mannose and glucosamine in a PtsG-dependent manner. By use of enhanced
growth on glucosamine for selection, four further sites were identified
where substitutions caused broadened substrate specificity (G176D,
A288V, G320S, and P384R). The altered amino acids include residues
previously identified as changing the uptake of ribose, fructose, and
mannitol. The mutations belonged to two classes. First, at two sites,
changes affected transmembrane residues (A288V and G320S), probably
altering sugar selectivity directly. More remarkably, the five other
specificity mutations affected residues unlikely to be in transmembrane
segments and were additionally associated with increased
ptsG transcription in the absence of glucose. Increased
expression of wild-type EIIGlc was not by itself sufficient
for growth with other sugars. A model is proposed in which the protein
conformation determining sugar accessibility is linked to
transcriptional signal transduction in EIIGlc. The
conformation of EIIGlc elicited by either glucose transport
in the wild-type protein or permanently altered conformation in the
second category of mutants results in altered signal transduction and
interaction with a regulator, probably Mlc, controlling the
transcription of pts genes.
*
Corresponding author. Mailing address: Department of
Microbiology G08, University of Sydney, Sydney, New South Wales 2006, Australia. Phone: (61-2)-9351-4277. Fax: (61-2)-9351-4571. E-mail: t.ferenci{at}microbio.usyd.edu.au.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»