The initiation mass for DNA replication in Escherichia coli K-12 is dependent on growth rate.

Wold, Sture; Skarstad, Kirsten; Steen, Harald B.; Stokke, Trond; Boye, Erik

doi:10.1002/j.1460-2075.1994.tb06485.x

Cited by 129 publications

(163 citation statements)

References 33 publications

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“…In E. coli, reducing the growth rate does reduce cell size (Schaechter et al, 1958) (Donachie, 1968). However, recent studies (Wold et al, 1994) We have clearly shown in this study that spnA95 is a mutation in the structural gene of the cysteinyl-tRNA synthetase, displaying highly conserved motifs characteristic of class I aminoacyl-tRNA synthetases and showing strong homology with E.coli cysteinyl-tRNA synthetase (47% identity over the entire sequence). Interestingly, the spnA495 mutation was shown by recombinational analysis to map in a 400 bp region (S.Casaregola et al, manuscript in preparation) which corresponds to the catalytic part of the cysteinyl-tRNA synthetase (CysRS).…”

Section: Resultsmentioning

confidence: 63%

A mutant cysteinyl-tRNA synthetase affecting timing of chromosomal replication initiation in B. subtilis and conferring resistance to a protein kinase C inhibitor.

et al. 1994

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A Bacilus subdlis mutant spnA95 was isolated as resistant at 30°C to the protein kinase C (PKC) inhibitor, sphinganine, and temperature sensitive for growth. As deduced by flow cytometry measurements, the mutant has a 35% reduced initiation mass at permissive temperature, resulting in initiation of DNA replication much earlier in the cell cycle than in the wild type. This modification is accompanied by a change in cell size, as determined by phase-contrast microscopy and flow cytometry. Therefore, this strain displays the characteristics of a novel cell clock mutant. spnA is a newly identified gene in B.subtilis and was shown to encode a cysteinyl-tRNA synthetase. At non-permissive temperature, the mutant was defective in the synthesis of P70, a protein with several characteristics of PKC (a cysteinerich protein). As one possibility, we propose that the altered timing of replication may be due to the reduced synthesis of specific cysteine-rich proteins normally involved in controlling chromosomal replication initiation in B.subtilis.

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Section: Resultsmentioning

confidence: 63%

A mutant cysteinyl-tRNA synthetase affecting timing of chromosomal replication initiation in B. subtilis and conferring resistance to a protein kinase C inhibitor.

et al. 1994

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“…The changing exponential rate of cell growth in varying media is thus not matched by similar changes in the linear replication rate; they are however coupled by frequencies: the frequency of initiations follows that of mass doublings. One should keep in mind that these values and constants are not 'sacred': they do change with t, more so at slow growth rates (Zaritsky & Zabrovitz, 1981;Wold et al, 1994), and can be manipulated by various means (e.g. Meacock & Pritchard, 1975;Wold et al, 1994).…”

Section: Growth Chromosome Replication and Cell Division -Coupling Amentioning

confidence: 99%

Instructive simulation of the bacterial cell division cycle

2011

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The coupling between chromosome replication and cell division includes temporal and spatial elements. In bacteria, these have globally been resolved during the last 40 years, but their full details and action mechanisms are still under intensive study. The physiology of growth and the cell cycle are reviewed in the light of an established dogma that has formed a framework for development of new ideas, as exemplified here, using the Cell Cycle Simulation (CCSim) program. CCSim, described here in detail for the first time, employs four parameters related to time (replication, division and inter-division) and size (cell mass at replication initiation) that together are sufficient to describe bacterial cells under various conditions and states, which can be manipulated environmentally and genetically. Testing the predictions of CCSim by analysis of time-lapse micrographs of Escherichia coli during designed manipulations of the rate of DNA replication identified aspects of both coupling elements. Enhanced frequencies of cell division were observed following an interval of reduced DNA replication rate, consistent with the prediction of a minimum possible distance between successive replisomes (an eclipse). As a corollary, the notion that cell poles are not always inert was confirmed by observed placement of division planes at perpendicular planes in monstrous and cuboidal cells containing multiple, segregating nucleoids.

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“…The parameters of the host strain (KH5402-1) bearing no plasmid were almost the same as those of pBR322-bearing cells (data not shown). Based on these results, the cell size at the time of initiation of chromosomal replication and so-called initiation mass (cell size at initiation per oriC) was calculated (Donachie, 1968;Wold et al, 1994): the relative size at initiation in pBR322-bearing and pMK11-bearing cells was 64.2 and 64.0, respectively, in the size unit shown in Fig. 7C, and the initiation mass was 16.0 in the same units for both, indicating no significant difference between the two.…”

Section: Division Inhibition Is Independent Of Sfiamentioning

confidence: 99%

“…Initiation of chromosome replication occurs at a specific time during the cell cycle (Donachie, 1968;Donachie and Robinson, 1987;Wold et al, 1994). Cell division occurs after a time lag (20 min when growth rate is 20-60 min) from completion of chromosome replication (Helmstetter, 1996).…”

Section: Introductionmentioning

confidence: 99%

CedA is a novel Escherichia coli protein that activates the cell division inhibited by chromosomal DNA over‐replication

Katayama

Takata

Sekimizu

1997

Molecular Microbiology

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SummaryWe isolated and characterized a new gene related to the control of cell division regulation in Escherichia coli. At 30ЊC, the dnaAcos mutant causes over-replication of the chromosome, and colony formation is inhibited. We found that, at this temperature, the dnaAcos cells form filaments; therefore, septum formation is inhibited. This inhibition was independent of SfiA, an inhibitor of the septum-forming protein, FtsZ. To identify factors involved in this pathway of inhibition, we isolated seven multicopy suppressors for the cold-sensitive phenotype of the dnaAcos mutant. One of these proved to be a previously unknown gene, which we named cedA. This gene encoded a 12 kDa protein and resided at 38.9 min on the E. coli genome map. A multicopy supply of the cedA gene to the dnaAcos cells did not repress over-replication of the chromosome but did stimulate cell division of the host, the result being growth of cells with an abnormally elevated chromosomal copy number. Therefore, the expression level of the cedA gene seems to be important for inhibiting cell division of the dnaAcos mutant at 30ЊC. We propose that overreplication of the chromosome activates a pathway for inhibiting cell division and that the cedA gene modulates this division control. In the dnaA þ background, cedA also seems to affect cell division.

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The initiation mass for DNA replication in Escherichia coli K-12 is dependent on growth rate.

Abstract: It is widely accepted that the initiation mass of Escherichia coli is constant and independent of growth rate, and therefore is an important parameter in the regulation of initiation of DNA replication. We

Cited by 129 publications

References 33 publications

A mutant cysteinyl-tRNA synthetase affecting timing of chromosomal replication initiation in B. subtilis and conferring resistance to a protein kinase C inhibitor.

A mutant cysteinyl-tRNA synthetase affecting timing of chromosomal replication initiation in B. subtilis and conferring resistance to a protein kinase C inhibitor.

Instructive simulation of the bacterial cell division cycle

CedA is a novel Escherichia coli protein that activates the cell division inhibited by chromosomal DNA over‐replication

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