Molecular cloning and functional characterization of a copy number control gene (copB) of plasmid R1

Riise, Erik; Stougaard, Peter; Bindslev, B; Nordström, Kurt; Molin, Søren

doi:10.1128/jb.151.3.1136-1145.1982

Cited by 40 publications

(13 citation statements)

References 33 publications

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“…It is not known at present whether the CopF/operator complex can also arrest transcription forks. Interestingly, repressers of plasmids Rl and pLSi (CopB and RepA, respectively) are not incompatibility determinants (Riise et al, 1982;del Solar and Espinosa, 1992). In Rl, this is owing to the fact that transcription of the rep gene is directed by two promoters, one being regulated by the repressor, the other being constitutive (Light and Molin, 1982;Rownd et ai, 1985).…”

Section: Discussionmentioning

confidence: 99%

The pAMβ1 CopF repressor regulates plasmid copy number by controlling transcription of the repE gene

Ehrlich

Janniere

1994

Molecular Microbiology

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pAM beta 1 is a low-copy-number, promiscuous plasmid from Gram-positive bacteria that replicates by a unidirectional theta-type mode. Its replication is initiated by an original mechanism, involving the positive rate-limiting RepE protein. Here we show that the pAM beta 1-encoded CopF protein is involved in negative regulation of the plasmid copy number. CopF represses approximately 10-fold the transcription initiated at the promoter of the repE gene and binds to a 31 bp segment which is located immediately upstream of the -35 box of the repE promoter. We propose that CopF inhibits initiation of transcription at the repE promoter by binding to its operator.

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Section: Discussionmentioning

confidence: 99%

The pAMβ1 CopF repressor regulates plasmid copy number by controlling transcription of the repE gene

Ehrlich

Janniere

1994

Molecular Microbiology

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“…The second copy number control element of plasmid R1 is the transcriptional repressor CopB. The deletion of copB results in an 8-fold copy number increase (156). The copB gene is cotranscribed with tap and repA from promoter pI.…”

Section: Inhibition Of Leader Peptide Translation: R1 and Related Plamentioning

confidence: 99%

Plasmid Replication Control by Antisense RNAs

Brantl

2014

Microbiol Spectr

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Plasmids are selfish genetic elements that normally constitute a burden for the bacterial host cell. This burden is expected to favor plasmid loss. Therefore, plasmids have evolved mechanisms to control their replication and ensure their stable maintenance. Replication control can be either mediated by iterons or by antisense RNAs. Antisense RNAs work through a negative control circuit. They are constitutively synthesized and metabolically unstable. They act both as a measuring device and a regulator, and regulation occurs by inhibition. Increased plasmid copy numbers lead to increasing antisense-RNA concentrations, which, in turn, result in the inhibition of a function essential for replication. On the other hand, decreased plasmid copy numbers entail decreasing concentrations of the inhibiting antisense RNA, thereby increasing the replication frequency. Inhibition is achieved by a variety of mechanisms, which are discussed in detail. The most trivial case is the inhibition of translation of an essential replication initiator protein (Rep) by blockage of the rep-ribosome binding site. Alternatively, ribosome binding to a leader peptide mRNA whose translation is required for efficient Rep translation can be prevented by antisense-RNA binding. In 2004, translational attenuation was discovered. Antisense-RNA-mediated transcriptional attenuation is another mechanism that has, so far, only been detected in plasmids of Gram-positive bacteria. ColE1, a plasmid that does not need a plasmid-encoded replication initiator protein, uses the inhibition of primer formation. In other cases, antisense RNAs inhibit the formation of an activator pseudoknot that is required for efficient Rep translation.

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“…These results, as well as those from in vivo data using fusion chimeras, indicate that the copB+ product inhibits transcription of repAL. In both types of experiment, the target of the copB product was found to lie within the 60base pair (bp) region containing the RNA II or RNA-A promoter (promoter 2 in When a copB+-containing plasmid that lacks the copA region is present, no effect on the copy number of a wild- type Rl plasmid is detectable, and there is no "switch off" of DNA replication in a host integratively suppressed by wildtype Ri (147). From this it was concluded that the addition of extra copB+ product has no significant effect on the wildtype plasmid, presumably because the copB target is already saturated in the wild-type state.…”

Section: Copb = Repa2mentioning

confidence: 99%