Clues to quality of journals
Open Access Policy of Helmholtz Association 2016
CC Licencences
Publication Metrics
Home
Deutsch
New EVA Application
Advanced Search
Browse by ...
Publication overview
Statistics (last 5 years)
OA Publications
Submit Publication
Import publication from...
Report missing publication
Contact persons
Help
Text
Endnote (RIS)
BibTeX
DOI
PMC
 |
|
Open Access Green as soon as Postprint is submitted to ZB.
A DNA architectural protein couples cellular physiology and DNA topology in Escherichia coli.
Mol. Microbiol. 34, 953-964 (1999)
In Escherichia coli, the transcriptional activity of many promoters is strongly dependent on the negative superhelical density of chromosomal DNA. This, in turn, varies with the growth phase, and is correlated with the overall activity of DNA gyrase, the major topoisomerase involved in the elevation of negative superhelicity. The DNA architectural protein FIS is a regulator of the metabolic reorganization of the cell during early exponential growth phase. We have previously shown that FIS modulates the superhelical density of plasmid DNA in vivo, and on binding reshapes the supercoiled DNA in vitro. Here, we show that, in addition, FIS represses the gyrA and gyrB promoters and reduces DNA gyrase activity. Our results indicate that FIS determines DNA topology both by regulation of topoisomerase activity and, as previously inferred, by directly reshaping DNA. We propose that FIS is involved in coupling cellular physiology to the topology of the bacterial chromosome.
Impact Factor
Scopus SNIP
Scopus
Cited By
Cited By
Altmetric
0.000
0.000
131
Annotations
Special Publikation
Hide on homepage
Publication type
Article: Journal article
Document type
Scientific Article
Language
english
Publication Year
1999
HGF-reported in Year
0
ISSN (print) / ISBN
0950-382x
e-ISSN
1365-2958
Journal
Molecular Microbiology
Quellenangaben
Volume: 34,
Issue: 5,
Pages: 953-964
Publisher
Wiley
Reviewing status
Peer reviewed
Institute(s)
Institute of Functional Epigenetics (IFE)
POF-Topic(s)
30203 - Molecular Targets and Therapies
Research field(s)
Helmholtz Diabetes Center
PSP Element(s)
G-502800-001
PubMed ID
10594821
Erfassungsdatum
1999-12-31