The initiator titration model: computer simulation of chromosome and minichromosome control

Hansen, Flemming; Christensen, Bjarke Bak; Atlung, Tove

doi:10.1016/0923-2508(91)90025-6

Cited by 158 publications

(187 citation statements)

References 28 publications

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“…The currently most accepted model considers that DnaA, the protein which binds the origin of replication oriC to promote the assembly of the replication complex, constitutes the initiator protein in E. coli and several authors have argued that a threshold concentration of DnaA has to be reached for initiation to take place (Lobner-Olesen et al, 1989;Hansen et al, 1991). However, several observations are difficult to reconcile with DnaA as the sole master regulator (see Bremer and Churchward, 1991).…”

Section: Introductionmentioning

confidence: 97%

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: Introductionmentioning

confidence: 97%

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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“…Alterations in DnaA concentration result in a variation of the time of initiation in the cell cycle (Loebner-Olesen et al, 1989). Models for initiation control postulate that DnaA accumulates to a critical level at which initiation occurs (Hansen et al, 1991). This implies that DnaA is itself intricately controlled, as will be discussed below.…”

Section: Introductionmentioning

confidence: 99%

DnaA initiator—also a transcription factor

Messer

Weigel

1997

Molecular Microbiology

143

126

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“…DnaA is thought to have a central role in controlling initiation timing as alterations in its concentration lead to changes in the initiation mass (LerbnerOlesen et al, 1989); also, certain dnaA mutations cause loss of initiation synchrony (Boye et a/., 1988). Models for the control of initiation postulate that DnaA, or an initiation-competent form of DnaA, must accumulate to a critical level to permit initiation; immediate re-initiation is thought to be prevented by the post-initiation sequestration of origins and the dnaA promoter (Campbell and Kleckner, 1990), or through sequestration or inactivation of DnaA protein (Hansen et a/., 1991 ;Katayama, 1994).…”

Section: Introductionmentioning

confidence: 99%

Autoregulation of the Escherichia coli replication initiator protein, DnaA, is indirect

Smith

McAteer

Masters

1997

Molecular Microbiology

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SummaryThe expression of dnaA is autoregulated, in that transcription of the gene increases when DnaA is inactivated (and initiation of replication prevented) and decreases when DnaA is supplied in excess. However, the inactivation of DnaA does not necessarily lead to increased DnaA production, as dnaA(Ts; temperature sensitive) strains which are integratively suppressed by derivatives of the plasmid R1 do not show temperatureinduced derepression. Several possible explanations for this unanticipated behaviour were considered and ruied out. We suggest here that the completion of a critical step in initiation may prevent dnaA derepression: although DnaA would be required t o complete this step at oriC, DnaA(Ts) would be sufficient at the R1 origin. Autoregulation of dnaA has been attributed to the binding of DnaA at a consensus binding site in the dnaA promoter region. We show here, using reporter systems, that this DnaA-binding site is not required for the autoregulatory response. We find, further, that replacement of the chromosomal dnaA gene with one containing a mutated binding site causes no demonstrable phenotypic change: cells with the mutant gene show no disadvantage in competition with dnaAf cells.

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The initiator titration model: computer simulation of chromosome and minichromosome control

Cited by 158 publications

References 28 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.

DnaA initiator—also a transcription factor

Autoregulation of the Escherichia coli replication initiator protein, DnaA, is indirect

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