Replication-induced transcription of an autorepressed gene: The replication initiator gene of plasmid P1

Mukhopadhyay, Suman; Chattoraj, Dhruba K.

doi:10.1073/pnas.130189497

Cited by 19 publications

(16 citation statements)

References 27 publications

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“…Fragments containing the rctB control region were obtained from N16961 by PCR amplification. The fragments were fused to the lacZ gene present in promoter and protein fusion vectors pMLB1109 (21) and pMLB1034 (31), respectively, and the resultant plasmids are described in Table 1. The identity of all cloned fragments was verified by DNA sequencing.…”

Section: Methodsmentioning

confidence: 99%

Multipartite Regulation ofrctB, the Replication Initiator Gene ofVibrio choleraeChromosome II

et al. 2005

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Replication initiator proteins in bacteria not only allow DNA replication but also often regulate the rate of replication initiation as well. The regulation is mediated by limiting the synthesis or availability of initiator proteins. The applicability of this principle is demonstrated here for RctB, the replication initiator for the smaller of the two chromosomes of Vibrio cholerae. A strong promoter for the rctB gene named rctBp was identified and found to be autoregulated in Escherichia coli. Promoter activity was lower in V. cholerae than in E. coli, and a part of this reduction is likely to be due to autorepression. Sequences upstream of rctBp, implicated earlier in replication control, enhanced the repression. The action of the upstream sequences required that they be present in cis, implying long-range interactions in the control of the promoter activity. A second gene specific for chromosome II replication, rctA, reduced rctB translation, most likely by antisense RNA control. Finally, optimal rctBp activity was found to be dependent on Dam. Increasing RctB in trans increased the copy number of a miniplasmid carrying oriCII VC , implying that RctB can be rate limiting for chromosome II replication. The multiple modes of control on RctB are expected to reduce fluctuations in the initiator concentration and thereby help maintain chromosome copy number homeostasis.

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Section: Methodsmentioning

confidence: 99%

Multipartite Regulation ofrctB, the Replication Initiator Gene ofVibrio choleraeChromosome II

et al. 2005

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“…It now appears that the primary mechanism of inhibition is by dimer-mediated handcuffing of iterons, the probability of which increases because of increased dimer concentrations due to increases in plasmid copy numbers. We note that, as speculated by Pritchard et al, in plasmid P1, new initiators are synthesized in a burst when replication initiates (18,29). (In Bacillus subtilis, the autorepressed initiator gene dnaA is also induced at the time of replication initiation [30].)…”

Section: Figmentioning

confidence: 95%

“…(In Bacillus subtilis, the autorepressed initiator gene dnaA is also induced at the time of replication initiation [30].) An elongating replication fork most likely dislodges the bound initiators from the promoter and thereby activates transcription ("replicationinduced transcription") (29). This causes a more sudden increase in the dimer-tomonomer (inhibitor-to-initiator) ratio.…”

Section: Figmentioning

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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“…When initiators are supplied in trans at a level only 2-fold below the physiological level, the plasmid copy number declines drastically (10). The copy number also falls when extra iterons are supplied in trans, but this drop can be overcome by supplying extra initiators (18,(26)(27)(28). Iteronmediated control thus can be sensitive to initiator concentration.…”

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confidence: 99%

Multiple homeostatic mechanisms in the control of P1 plasmid replication

Das

Valjavec-Gratian

Basuray

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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Many organisms control initiation of DNA replication by limiting supply or activity of initiator proteins. In plasmids, such as P1, initiators are limited primarily by transcription and dimerization. However, the relevance of initiator limitation to plasmid copy number control has appeared doubtful, because initiator oversupply increases the copy number only marginally. Copy number control instead has been attributed to initiator-mediated plasmid pairing (''handcuffing''), because initiator mutations to handcuffing deficiency elevates the copy number significantly. Here, we present genetic evidence of a role for initiator limitation in plasmid copy number control by showing that autorepression-defective initiator mutants also can elevate the plasmid copy number. We further show, by quantitative modeling, that initiator dimerization is a homeostatic mechanism that dampens active monomer increase when the protein is oversupplied. This finding implies that oversupplied initiator proteins are largely dimeric, partly accounting for their limited ability to increase copy number. A combination of autorepression, dimerization, and handcuffing appears to account fully for control of P1 plasmid copy number.autorepression ͉ DNA replication control ͉ homeostatic control ͉ plasmid copy number control

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Replication-induced transcription of an autorepressed gene: The replication initiator gene of plasmid P1

Cited by 19 publications

References 27 publications

Multipartite Regulation ofrctB, the Replication Initiator Gene ofVibrio choleraeChromosome II

Multipartite Regulation ofrctB, the Replication Initiator Gene ofVibrio choleraeChromosome II

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

Multiple homeostatic mechanisms in the control of P1 plasmid replication

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