The Terminus of Chromosome Replication of E. coli Phenotypic Suppression of a dnaA Mutation by Plasmid Integration near terC

1983 ◽  
pp. 247-263 ◽  
Author(s):  
Jacqueline Louarn ◽  
Philippe Legrand ◽  
Josette Patte ◽  
Jean-Michel Louarn
Keyword(s):  
Chromosome Replication ◽  
E Coli ◽  
Plasmid Integration ◽  
Phenotypic Suppression ◽  
Dnaa Mutation

A cold sensitive dnaA mutant of E. coli which overinitiates chromosome replication at low temperature

1978 ◽  
Vol 162 (1) ◽  
pp. 9-16 ◽  
Author(s):  
G. Kellenberger-Gujer ◽  
A. J. Podhajska ◽  
L. Caro
Keyword(s):  
Low Temperature ◽  
Chromosome Replication ◽  
E Coli ◽  
Dnaa Mutant ◽  
Cold Sensitive

scholarly journals Multiple DNA Binding Proteins Contribute to Timing of Chromosome Replication in E. coli

2016 ◽  
Vol 3 ◽  
Author(s):  
Leise Riber ◽  
Jakob Frimodt-Møller ◽  
Godefroid Charbon ◽  
Anders Løbner-Olesen
Keyword(s):  
Dna Binding ◽  
Binding Proteins ◽  
Dna Binding Proteins ◽  
Chromosome Replication ◽  
E Coli

Replication of the bacterial chromosome

1966 ◽  
Vol 164 (995) ◽  
pp. 258-266 ◽  
Keyword(s):  
Escherichia Coli ◽  
Cell Division ◽  
Rapid Growth ◽  
Chromosome Replication ◽  
E Coli ◽  
Initiation Of Replication ◽  
Replication Point ◽  
Generation Times ◽  
Minimal Media ◽  
Resting Period

In this paper I shall confine myself to only one aspect of chromosome replication in bacteria: its control and co-ordination with growth and cell division. The nature of the problem to be considered is made clear by two features of chromosome replication in Escherichia coli , First, under conditions of rapid growth, involving generation times of up to about one hour, DNA synthesis is essentially continuous; there is no detectable resting period corresponding to the G period typically found in higher organisms. Secondly, in glucose minimal media, as the data of Cairns (1963) and others have shown, a single replication point, or growth point, traverses the length of the chromosome during each cycle of replication. It follows that, although the rate of replication in E. coli might be determined by the supply of DNA precursors, the maintenance of the proper sequence of events cannot be controlled in this way since in a system in which DNA synthesis is continuous these precursors must be present at all times. Under the conditions mentioned above in E. coli , for example, the cell must have some means of ensuring that a new cycle of replication is not initiated until the previous one is complete. Consequently the important point of control of replication in bacteria must be over the initiation of replication rather than replication itself.

scholarly journals PriA Is Essential for Viability of the Escherichia coli Topoisomerase IV parE10(Ts) Mutant

2004 ◽  
Vol 186 (4) ◽  
pp. 1197-1199 ◽  
Author(s):  
Gianfranco Grompone ◽  
Vladimir Bidnenko ◽  
S. Dusko Ehrlich ◽  
Bénédicte Michel
Keyword(s):  
Escherichia Coli ◽  
Chromosome Replication ◽  
Topoisomerase Iv ◽  
E Coli ◽  
Replication Restart ◽  
Independent Replication ◽  
Ts Mutant

ABSTRACT The parE10(Ts) mutation, which renders Escherichia coli thermosensitive for growth by inactivation of the essential E. coli topoisomerase topo IV, is lethal at all temperatures when PriA, the main replication restart protein, is absent. This lethality is suppressed by the activation of a PriA-independent replication restart pathway (dnaC809 mutation). This result suggests that topo IV acts prior to full-chromosome replication completion.

scholarly journals Blocking, Bending, and Binding: Regulation of Initiation of Chromosome Replication During the Escherichia coli Cell Cycle by Transcriptional Modulators That Interact With Origin DNA

2021 ◽  
Vol 12 ◽  
Author(s):  
Julia E. Grimwade ◽  
Alan C. Leonard
Keyword(s):  
Escherichia Coli ◽  
Cell Cycle ◽  
Chromosome Replication ◽  
Integration Host Factor ◽  
Replication Initiation ◽  
Critical Event ◽  
E Coli ◽  
Chromosome Duplication ◽  
Recognition Sites ◽  
Transcriptional Modulators

Genome duplication is a critical event in the reproduction cycle of every cell. Because all daughter cells must inherit a complete genome, chromosome replication is tightly regulated, with multiple mechanisms focused on controlling when chromosome replication begins during the cell cycle. In bacteria, chromosome duplication starts when nucleoprotein complexes, termed orisomes, unwind replication origin (oriC) DNA and recruit proteins needed to build new replication forks. Functional orisomes comprise the conserved initiator protein, DnaA, bound to a set of high and low affinity recognition sites in oriC. Orisomes must be assembled each cell cycle. In Escherichia coli, the organism in which orisome assembly has been most thoroughly examined, the process starts with DnaA binding to high affinity sites after chromosome duplication is initiated, and orisome assembly is completed immediately before the next initiation event, when DnaA interacts with oriC’s lower affinity sites, coincident with origin unwinding. A host of regulators, including several transcriptional modulators, targets low affinity DnaA-oriC interactions, exerting their effects by DNA bending, blocking access to recognition sites, and/or facilitating binding of DnaA to both DNA and itself. In this review, we focus on orisome assembly in E. coli. We identify three known transcriptional modulators, SeqA, Fis (factor for inversion stimulation), and IHF (integration host factor), that are not essential for initiation, but which interact directly with E. coli oriC to regulate orisome assembly and replication initiation timing. These regulators function by blocking sites (SeqA) and bending oriC DNA (Fis and IHF) to inhibit or facilitate cooperative low affinity DnaA binding. We also examine how the growth rate regulation of Fis levels might modulate IHF and DnaA binding to oriC under a variety of nutritional conditions. Combined, the regulatory mechanisms mediated by transcriptional modulators help ensure that at all growth rates, bacterial chromosome replication begins once, and only once, per cell cycle.

scholarly journals Growth Rate of Escherichia coli During Human Urinary Tract Infection: Implications for Antibiotic Effect

Antibiotics ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 92 ◽  
Author(s):  
Haugan ◽  
Hertz ◽  
Charbon ◽  
Sahin ◽  
Løbner-Olesen ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Growth Rate ◽  
Urinary Tract Infection ◽  
Urinary Tract ◽  
Bacterial Growth ◽  
Chromosome Replication ◽  
Bacterial Growth Rate ◽  
E Coli ◽  
Antibiotic Effect

Escherichia coli is the primary cause of urinary tract infection (UTI), which is one of the most frequent human infections. While much is understood about the virulence factors utilized by uropathogenic E. coli (UPEC), less is known about the bacterial growth dynamics taking place during infection. Bacterial growth is considered essential for successful host colonization and infection, and most antibiotics in clinical use depend on active bacterial growth to exert their effect. However, a means to measure the in situ bacterial growth rate during infection has been lacking. Due to faithful coordination between chromosome replication and cell growth and division in E. coli, chromosome replication provides a quantitative measure of the bacterial growth rate. In this study, we explored the potential for inferring in situ bacterial growth rate from a single urine sample in patients with E. coli bacteriuria by differential genome quantification (ori:ter) performed by quantitative PCR. We found active bacterial growth in almost all samples. However, this occurs with day-to-day and inter-patient variability. Our observations indicate that chromosome replication provides not only a robust measure of bacterial growth rate, but it can also be used as a means to evaluate antibiotic effect.

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