Plasmid-associated virulence of Salmonella enteritidis

Hovi, Marianne; Sukupolvi, Soila; Edwards, Mary F.; Rhen, Mikael

doi:10.1016/0882-4010(88)90066-6

Cited by 58 publications

(23 citation statements)

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“…Screening different Salmonella serovars with a pSDL2-specific recombination assay revealed that only strains harboring a virulence plasmid encode for resolvase activity. Our results suggest that site-specific recombination contributes to the stable inheritance of pSDL2 and other Salmonella virulence plasmids.The Salmonella dublin virulence plasmid pSDL2 and the closely related plasmids of certain other nontyphoidal Salmonella serotypes encode essential virulence determinants that enable the bacteria to produce systemic salmonellosis in mice (23,25,27,28). Although these plasmids are large and are present in only a few copies per cell, their estimated loss is less than 10-7 per generation per cell, suggesting the presence of an efficient stability system (12, 48).…”

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“…The Salmonella dublin virulence plasmid pSDL2 and the closely related plasmids of certain other nontyphoidal Salmonella serotypes encode essential virulence determinants that enable the bacteria to produce systemic salmonellosis in mice (23,25,27,28). Although these plasmids are large and are present in only a few copies per cell, their estimated loss is less than 10-7 per generation per cell, suggesting the presence of an efficient stability system (12, 48).…”

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Identification of a multimer resolution system involved in stabilization of the Salmonella dublin virulence plasmid pSDL2

Krause

Guiney

1991

J Bacteriol

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The Salmonella dublin virulence plasmid pSDL2 is a low-copy-number plasmid that is highly conserved in its host. Deletion of the 8-kb EcoRI C fragment downstream of the virulence region leads to plasmid instability and formation of multimers. We identified a multimer resolution system in the EcoRI C fragment composed of a trans-acting resolvase gene and a cis-acting resolution site. The resolvase gene, rsd, maps within a 2-kb EcoRV fragment and appears to be part of a multicistronic unit together with at least two other genes of unknown function. The derived protein, 28.7-kDa in size, is almost identical to the D protein of miniF. The C-terminal region was shown to have substantial similarity to the conserved C-terminal domains of the site-specific recombinases of the integrase family. The cis-acting resolution site, crs, is located upstream of rsd within a 628-bp SmaI-HpaI fragment. It contains eight direct incomplete 17-bp repeats followed by a segment rich in indirect repeats, the latter being homologous to the oriVI sequence of miniF. crs contains the crossover site for specific recombination and mediates bidirectional promoter activity. A replicative function in analogy to that of oriVi of F could not be demonstrated. The multimer resolution system was shown to stabilize pACYC184 and is dependent on the recA-mediated formation of multimeric plasmids. Screening different Salmonella serovars with a pSDL2-specific recombination assay revealed that only strains harboring a virulence plasmid encode for resolvase activity. Our results suggest that site-specific recombination contributes to the stable inheritance of pSDL2 and other Salmonella virulence plasmids.The Salmonella dublin virulence plasmid pSDL2 and the closely related plasmids of certain other nontyphoidal Salmonella serotypes encode essential virulence determinants that enable the bacteria to produce systemic salmonellosis in mice (23,25,27,28). Although these plasmids are large and are present in only a few copies per cell, their estimated loss is less than 10-7 per generation per cell, suggesting the presence of an efficient stability system (12, 48). Studies of stability strategies in other low-copy-number plasmids have identified partition systems, coupled cell division functions, postsegregational killing of plasmid-free cells, and multimer resolution functions. These mechanisms, acting individually or in combination, prevent the formation of plasmid-free segregants after cell division. The main principle of partition systems is thought to be an active physical separation of plasmid molecules into daughter cells that is analogous to the mitotic segregation of chromosomes (3). Coupled cell division and postsegregational killing involve similar but not identical mechanisms that select against plasmid-free cells (15,26,35). The plasmid encodes a potent cell-killing agent that destroys the plasmid-free segregants, while cells which retain the plasmid are protected by a plasmid-encoded antidote. Multimer resolution systems act by conversion of multime...

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confidence: 99%

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Identification of a multimer resolution system involved in stabilization of the Salmonella dublin virulence plasmid pSDL2

Krause

Guiney

1991

J Bacteriol

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“…Two of the 18 S. enteritidis strains studied showed no reaction ( Table 1), proving that for a given serovar known to contain virulence-related plasmids [4,8,[26][27], there is diversity. This was also confirmed for S. abortuas ovis, since only one of the two tested strains possessed the plasmid gene associated with virulence (Table 1) and for S. typhimuriam, since only 2 of the 20 tested strains did not respond to amplification (Table 1).…”

Section: Discussionmentioning

confidence: 99%

Polymerase chain reaction for salmonella virulence–associated plasmid genes detection: a new tool in salmonella epidemiology

Rexach¹,

Dilasser²,

Fach³

1994

Epidemiol. Infect.

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SUMMARYThe important role of plasmid genes in assessing virulence for BALB/c mice in salmonella, and the difficulty of using standard techniques to detect them, led us to develop a detection method by gene amplification.One hundred and forty-three strains (71 serovars) of salmonella and 35 strains of other species were tested using specific oligonucleotide primers. The amplification products were identified by a specific oligonucleotide probe. Forty-nine salmonella strains from ten serovars (S. abortus ovis, S. choleraesuis, S. dublin, S. enteritidis, S. gallinarum/pullorum, S. hessarek, S. typhimurium, S. IIIa 48: Z4, Z23, S. IV43:z4, Z23: -, S. V 28: a: -) produced a positive and specific response.Because of various origins of the strains possessing the gene sought and the diversity of the responses, both from one serovar to another and in the same serovar, this search has its place among the epidemiological markers in general use. This method appears well suited to the research and detection of plasmid genes associated with mouse virulence in salmonella.

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“…Furthermore, elimination of the resident plasmids is spontaneous; therefore, screening colonies for plasmid-cured strains is a tedious process. Finally, most known plasmid-curing chemical agents are toxic or mutagenic (e.g., acridine orange, ethidium bromide, and sodium dodecyl sulfate) and can therefore induce mutations in the host chromosome [17]. Mutations also occur during harsh physical curing treatments (e.g., high temperature or UV light).…”

Section: Introductionmentioning

confidence: 99%

Curing of Plasmid pXO1 from Bacillus anthracis Using Plasmid Incompatibility

Liu¹,

Wang²,

Wang³

et al. 2012

PLoS ONE

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The large plasmid pXO1 encoding the anthrax toxin is important for the virulence of Bacillus anthracis. It is essential to cure pXO1 from B. anthracis to evaluate its role in the pathogenesis of anthrax infection. Because conventional methods for curing plasmids (e.g., curing agents or growth at elevated temperatures) can induce mutations in the host chromosomal DNA, we developed a specific and reliable method to eliminate pXO1 from B. anthracis using plasmid incompatibility. Three putative replication origins of pXO1 were inserted into a temperature-sensitive plasmid to generate three incompatible plasmids. One of the three plasmids successfully eliminated the large plasmid pXO1 from B. anthracis vaccine strain A16R and wild type strain A16. These findings provided additional information about the replication/partitioning of pXO1 and demonstrated that introducing a small incompatible plasmid can generate plasmid-cured strains of B. anthracis without inducing spontaneous mutations in the host chromosome.

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Plasmid-associated virulence of Salmonella enteritidis

Cited by 58 publications

References 23 publications

Identification of a multimer resolution system involved in stabilization of the Salmonella dublin virulence plasmid pSDL2

Identification of a multimer resolution system involved in stabilization of the Salmonella dublin virulence plasmid pSDL2

Polymerase chain reaction for salmonella virulence–associated plasmid genes detection: a new tool in salmonella epidemiology

Curing of Plasmid pXO1 from Bacillus anthracis Using Plasmid Incompatibility

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