Random initiation of replication of plasmids P1 and F (oriS) when integrated into the Escherichia coli chromosome

Eliasson, Åsa; Bernander, Rolf; Nordström, Kurt

doi:10.1111/j.1365-2958.1996.tb02543.x

Cited by 16 publications

(17 citation statements)

References 32 publications

(31 reference statements)

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“…Deletion of the L-13-mer made oriC inactive and could be rescued only by integrative suppression. To test the induction of HIR in a mutant bacterium, we used strain CM735 intFs-B, in which the L-13-mer was replaced by a mini-F plasmid (8). No HIR was detected in this strain (Table 3).…”

Section: Resultsmentioning

confidence: 99%

Initiation of Heat-Induced Replication Requires DnaA and the L-13-mer of oriC

2006

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An upshift of 10°C or more in the growth temperature of an Escherichia coli culture causes induction of extra rounds of chromosome replication. This stress replication initiates at oriC but has functional requirements different from those of cyclic replication. We named this phenomenon heat-induced replication (HIR). Analysis of HIR in bacterial strains that had complete or partial oriC deletions and were suppressed by F integration showed that no sequence outside oriC is used for HIR. Analysis of a number of oriC mutants showed that deletion of the L-13-mer, which makes oriC inactive for cyclic replication, was the only mutation studied that inactivated HIR. The requirement for this sequence was strictly correlated with Benham's theoretical stressinduced DNA duplex destabilization. oriC mutations at DnaA, FIS, or IHF binding sites showed normal HIR activation, but DnaA was required for HIR. We suggest that strand opening for HIR initiation occurs due to heat-induced destabilization of the L-13-mer, and the stable oligomeric DnaA-single-stranded oriC complex might be required only to load the replicative helicase DnaB.The initiation of chromosome replication is the central event in the bacterial cell cycle and the step that controls the frequency with which chromosomes are replicated. Initiation is a precisely timed event that occurs once during the cell cycle. In Escherichia coli replication initiates at a unique site, oriC, located at min 84.5 on the genetic map. The minimal sequence that promotes replication was found to be 258 bp long (25). The left side of oriC is an AT-rich region consisting of an AT cluster and three similar sequences, each 13 nucleotides long and each starting with GATC

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Section: Resultsmentioning

confidence: 99%

Initiation of Heat-Induced Replication Requires DnaA and the L-13-mer of oriC

2006

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“…Minichromosome replication in an intPl host 121 7 normal cell-cycle-specific control (Eliasson et a/., 1996b;Nordstrom et a/., 1991). The fact that chromosome replication in int strains is random in time was used to distinguish between the two modes of control of minichromosome replication.…”

Section: Discussionmentioning

confidence: 99%

“…The density-shift experiment was performed essentially as described previously (Eliasson et a/., 1996b;Koppes and von Meyenburg, 1987), except that more label was incorporated into the DNA; 10 pCi ml-' of [3H]-methyl-thymidine 0 1997 Blackwell Science Ltd, Molecular Microbiology, 23, [1215][1216][1217][1218][1219][1220] …”

Section: Density Shiftmentioning

confidence: 99%

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Replication of minichromosomes in a host in which chromosome replication is random

Eliasson

Nordström

1997

Molecular Microbiology

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SummaryMinichromosomes are plasmids with the origin of chromosome replication, oriC, as their only origin of replication. In Escherichia coli, minichromosomes are compatible with the chromosome and replicate in a cell-cycle-specific manner at the same time as oriC located on the chromosome initiates replication. In int strains, oriC has been inactivated and replaced by a plasmid origin. Because plasmids control their own replication, chromosome replication is uncoupled from the normal cell-cycle control and is random with respect to the cell cycle in the int strains. We have used an intP7 strain to address thequestion of whether minicromosome replication i s coupled to the replication of the chromosome or is governed by cellcycle-specific signals. Minichromosome replication was analysed by density-shift experiments and found not to be random in the randomly replicating intP7 host. This suggests that the cell-cycle-specific control functions of oriC replication are operating also in the intP7 strain.

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“…For chromosomes, it appears that their large size necessitates controlling the timing of replication initiation for the timely completion of the cell cycle. However, integrated plasmids are in some circumstances able to ensure chromosome replication and cell viability in the absence of the normal replication system (integrative suppression) (12), at the price of discoordination with the cell cycle, leading to long interdivision times, cell shape abnormality, and slow growth (13,14). One question that we focus on here is how the natural plasmid-like replicons of secondary chromosomes behave, i.e., whether they overcome the lack of timing of the original plasmids and link replication to the cell cycle.…”

Section: Introduction Fmentioning

confidence: 99%

Random versus Cell Cycle-Regulated Replication Initiation in Bacteria: Insights from Studying Vibrio cholerae Chromosome 2

Ramachandran

Jha

Paulsson

et al. 2017

Microbiol Mol Biol Rev

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SUMMARY Bacterial chromosomes initiate replication at a fixed time in the cell cycle, whereas there is generally no particular time for plasmid replication initiation or chromosomal replication initiation from integrated plasmids. In bacteria with divided genomes, the replication system of one of the chromosomes typically resembles that of bacteria with undivided genomes, whereas the remaining chromosomes have plasmid-like replication systems. For example, in Vibrio cholerae, a bacterium with two chromosomes (chromosome 1 [Chr1] and Chr2), the Chr1 system resembles that of the Escherichia coli chromosome, and the Chr2 system resembles that of iteron-based plasmids. However, Chr2 still initiates replication at a fixed time in the cell cycle and thus offers an opportunity to understand the molecular basis for the difference between random and cell cycle-regulated modes of replication. Here we review studies of replication control in Chr2 and compare it to those of plasmids and chromosomes. We argue that although the Chr2 control mechanisms in many ways are reminiscent of those of plasmids, they also appear to combine more regulatory features than are found on a typical plasmid, including some that are more typical of chromosomes. One of the regulatory mechanisms is especially novel, the coordinated timing of replication initiation of Chr1 and Chr2, providing the first example of communication between chromosomes for replication initiation.

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Random initiation of replication of plasmids P1 and F (oriS) when integrated into the Escherichia coli chromosome

Cited by 16 publications

References 32 publications

Initiation of Heat-Induced Replication Requires DnaA and the L-13-mer of oriC

Initiation of Heat-Induced Replication Requires DnaA and the L-13-mer of oriC

Replication of minichromosomes in a host in which chromosome replication is random

Random versus Cell Cycle-Regulated Replication Initiation in Bacteria: Insights from Studying Vibrio cholerae Chromosome 2

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