Plasmid incompatibility and control of replication: copy mutants of the R-factor R1 in Escherichia coli K-12

Uhlin, Bernt Eric; Nordström, Kurt

doi:10.1128/jb.124.2.641-649.1975

Cited by 168 publications

(40 citation statements)

References 43 publications

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“…Miniplasmids from copy mutants of plasmid Rldrd-19. Previously, several copy mutants of Rldrd-19 were isolated ranging in copy numbers from 1 to 10 times the copy number of Rldrd-19 (37,38). Many of these mutant plasmids show a tendency to dissociate into smaller plasmids carrying only a few or none of the resistance genes in addition to a replicative origin (13; our unpublished data).…”

Section: Resultsmentioning

confidence: 87%

“…Incompatibility and stability. The phenomenon of incompatibility has been claimed to be part of the copy number control mechanism (37). Because our results strongly suggest that all genes involved in copy number control of plasmid Rldrd-19 are located close to the replication origin, we also analyzed the small plasmid derivatives for incompatibility properties.…”

Section: Resultsmentioning

confidence: 98%

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Clustering of genes involved in replication, copy number control, incompatibility, and stable maintenance of the resistance plasmid R1drd-19

Molin¹,

Stougaard²,

Uhlin³

et al. 1979

J Bacteriol

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Plasmid R1drd-19 is present in a small number of copies per cell of Escherichia coli. The plasmid was reduced in size by in vivo as well as in vitro (cloning) techniques, resulting in a series of plasmid derivatives of different molecular weight. All plasmids isolated contain a small region (about 2 x 10(6) daltons of deoxyribonucleic acid) of the resistance transfer factor part of the plasmid located close to one of the IS1 sequences that separates the resistance transfer factor part from the resistance determinant. All these derivatives were present at the same copy number, retained the incompatibility properties of plasmid R1drd-19, and were stably maintained during cell division. Genes mutated to yield copy mutations also were found to be located in the same region.

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Section: Resultsmentioning

confidence: 87%

Section: Resultsmentioning

confidence: 98%

Clustering of genes involved in replication, copy number control, incompatibility, and stable maintenance of the resistance plasmid R1drd-19

Molin¹,

Stougaard²,

Uhlin³

et al. 1979

J Bacteriol

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“…This is a simplifying assumption that will obviously have to be re-examined in future research, where we anticipate developing more accurate models that allow for variable plasmid numbers in the bacterial cell. The basis for this assumption derives from the observation that plasmids of similar compatibility classes cannot co-exist in the same cell (Novick 1987; Norman et al 2009), and that bacteria can control the number of plasmids in the cell (Uhlin and Nordstrom 1975; Novick 1987; Park et al 2001).…”

Section: Methodsmentioning

confidence: 99%

The Effect of Horizontal Gene Transfer on the Dynamics of Antibiotic Drug Resistance in a Unicellular Population with a Dynamic Fitness Landscape, Repression and De-repression

Atsmon-Raz

Wagner

2015

Preprint

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Antibiotic drug resistance spreads through horizontal gene transfer (HGT) via bacterial conjugation in unicellular populations of bacteria. Consequently, the efficiency of antibiotics is limited and the expected "grace period" of novel antibiotics is typically quite short. One of the mechanisms that allow the accelerated adaptation of bacteria to antibiotics is bacterial conjugation. However, bacterial conjugation is regulated by several biological factors, with one of the most important ones being repression and derepression.In recent work, we have studied the effects that repression and de-repression on the mutation-selection balance of an HGT-enabled bacterial population in a static environment. Two of our main findings were that conjugation has a deleterious effect on the mean fitness of the population and that repression is expected to allow a restoration of the fitness cost due to plasmid hosting.Here, we consider the effect that conjugation-mediated HGT has on the speed of adaptation in a dynamic environment and the effect that repression will have on the dynamics of antibiotic drug resistance. We find that, the effect of repression is dynamic in its possible outcome, that a conjugators to non-conjugators phase transition exists in a dynamic landscape as we have previously found for a static landscape and we quantify the time required for a unicellular population to adapt to a new antibiotic in a periodically changing fitness landscape. Our results also confirmed that HGT accelerates adaptation for a population of prokaryotes which agrees with current knowledge, that HGT rates increase when a population is put under stress.

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“…Fr., .....I VOL. 160,1984 on July 15, 2020 by guest http://jb.asm.org/ Downloaded from (pSC138 and its derivatives) was determined by measuring specific activity of ,-lactamase by the published procedure (22) or by determining "single-cell resistance" to ampicillin, as defined by Uhlin and Nordstrom (31).…”

Section: _imentioning

confidence: 99%

Control of F plasmid replication by a host gene: evidence for interaction of the mafA gene product of Escherichia coli with the mini-F incC region

Wada¹,

Yura²

1984

J Bacteriol

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Replication of F (including mini-F) and some related plasmids is known to be specifically inhibited in mafA mutants of Escherichia coli K-12. We have now isolated and characterized mini-F mutants that can overcome the replication inhibition. Such plasmids, designated pom (permissive on maJ), were obtained spontaneously or after mutagenesis with hydroxylamine or by transposon (Tn3) insertion. In addition to their ability to replicate in mafA mutant bacteria, the pom mutant plasmids exhibjt an increased copy number and resistance to "curing" by acridine dye in the mafA+ host. In agreement with these results, Tn3-induced pom mutants were found to carry Tn3 inserted at the incC region of mini-F DNA, known to be involved in incompatibility, control of copy number, and sensitivity to acridine dye. Furthermore, three of the seven mini-F plasmids tested that carry Tn3 within the tandem repeat sequences of the incC region (previously isolated by other workers) exhibit all the phenotypes of pom plasmids, the ability to replicate in the mafA strain, and high copy number and acridine resistance in the mafA+ strain. The rest of the plasmids that contain Tn3 just outside the tandem repeats remain wild type in all these properties. These results strongly suggest that the putative mafA gene product of host bacteria controls mini-F replication through interaction with the incC region.

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Plasmid incompatibility and control of replication: copy mutants of the R-factor R1 in Escherichia coli K-12

Cited by 168 publications

References 43 publications

Clustering of genes involved in replication, copy number control, incompatibility, and stable maintenance of the resistance plasmid R1drd-19

Clustering of genes involved in replication, copy number control, incompatibility, and stable maintenance of the resistance plasmid R1drd-19

The Effect of Horizontal Gene Transfer on the Dynamics of Antibiotic Drug Resistance in a Unicellular Population with a Dynamic Fitness Landscape, Repression and De-repression

Control of F plasmid replication by a host gene: evidence for interaction of the mafA gene product of Escherichia coli with the mini-F incC region

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