A Chromosomal Locus Which Controls the Ability of
            <i>Shigella flexneri</i>
            to Evoke Keratoconjunctivitis

Formal, Samuel B.; Gemski, P.; Baron, L. S.; LaBrec, E. H.

doi:10.1128/iai.3.1.73-79.1971

Cited by 105 publications

(34 citation statements)

References 13 publications

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“…However, it was interesting to note that a plasmid of about 4'0 to 4'2 Kb was found in serotypes 1-4, as was reported from Asia [21]. Genetic analysis has established that virulence in S. flexneri is associated with chromosomal loci [23]. In addition, a large plasmid of about 217 Kb has been observed [24,25].…”

mentioning

confidence: 64%

Molecular epidemiology of plasmid patterns inShigella flexneritypes 1–6

Gebre-Yohannes

Drašar

1991

Epidemiol. Infect.

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A total of 123 drug-resistant and drug-sensitive Shigella flexneri types 1-6, and their Escherichia coli K12 transconjugants were used for plasmid profile analysis by agarose gel electrophoresis. Resistance factors (R-factors) were further characterized by incompatibility testing. The overall distribution of small plasmids in S. flexneri showed that a cryptic plasmid of about 4.6 Kb was found in all serotypes, and a plasmid of about 4.2 Kb was found in serotypes 1-4. Shigella flexneri types 2, 4 and 6 showed a 6.5 Kb plasmid which correlated with SSu-resistance. All S. flexneri serotypes harboured large plasmids of about 217 Kb. Plasmid profile analysis of S. flexneri in Ethiopia showed a high degree of uniformity within individual serotypes. However, there was a limited variability which, at times, could be useful for epidemiological investigation. Shigella flexneri serotypes 1-6 harboured resistance plasmids with diverse molecular weights but mostly belonging to incompatibility groups N and X.

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mentioning

confidence: 64%

Molecular epidemiology of plasmid patterns inShigella flexneritypes 1–6

Gebre-Yohannes

Drašar

1991

Epidemiol. Infect.

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“…Formal and coworkers identified kcpA, a chromosomal gene in S. flexneri 2a that is required for the ability of the bacteria to provoke keratoconjunctivitis in a guinea-pig model for Shigella virulence (Formal et al, 1971). When S. flexneri 2a was mated with E. coli K-12 and the kcpA region was replaced with the homologous region from E. coli, the S. flexneri transconjugants lost the ability to produce keratoconjunctivitis.…”

Section: Additional Pathoadaptive Mutations and Antivirulence Genes Fmentioning

confidence: 99%

Black holes, antivirulence genes, and gene inactivation in the evolution of bacterial pathogens

Maurelli

2007

FEMS Microbiology Letters

132

116

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The evolution of bacterial pathogens from nonpathogenic ancestors is marked principally by the acquisition of virulence gene clusters on plasmids and pathogenicity islands via horizontal gene transfer. The flip side of this evolutionary force is the equally important adaptation of the newly minted pathogen to its new host niche. Pathoadaptive mutations take the form of modification of gene expression such that the pathogen is better fit to survive within the new niche. This mini-review describes the concept of pathoadaptation by loss of gene function. In this process, genes that are no longer compatible with the novel lifestyle of the pathogen are selectively inactivated either by point mutation, insertion, or deletion. These genes are called 'antivirulence genes'. Selective pressure sometimes leads to the deletion of large regions of the genome that contain antivirulence genes generating 'black holes' in the pathogen genome. Inactivation of antivirulence genes leads to a pathogen that is highly adapted to its host niche. Identification of antivirulence genes for a particular pathogen can lead to a better understanding of how it became a pathogen and the types of genetic traits that need to be silenced in order for the pathogen to colonize its new host niche successfully.

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“…Wild-type S. flexneri 2a YSH6000 (Sasakawa et al, 1986), its antibiotic-sensitive derivative YSH6000T (Nakata et al, 1992) and its plasmid-cured variant YSH6200 (Sasakawa et al, 1988) were used together with the virulent strain 2457T (Formal et al, 1971). Strains TC501 and N1436, the congenic tgt::Tn5 derivatives of YSH6000T and YSH6000, respectively, have been described earlier as well as plasmids pJD100, pJD102, pJD103 and pJD104 (Durand et al, 1994) and the virF ¢::¢lacZ fusion-bearing plasmid pHW848 (Nakayama and Watanabe, 1995).…”

Section: Bacterial Strains and Plasmidsmentioning

confidence: 99%

Putrescine or a combination of methionine and arginine restores virulence gene expression in a tRNA modification‐deficient mutant of Shigella flexneri: a possible role in adaptation of virulence

Durand

Björk²

2003

Molecular Microbiology

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SummaryThe wild-type strain YSH6000 of Shigella flexneri growing in minimal medium contains the modified nucleoside epoxy-Q (oQ) in a subset of tRNAs. This nucleoside is lacking in tRNA from a tgt mutant of this bacterium. When these bacteria are growing in minimal medium, the expression of virulence genes is 10-fold lower in the tgt mutant than in the wild type, although only a twofold reduction in the expression of these virulence factors is observed in broth. Such a strong media-dependant expression of virulence genes was not observed in the wild type. Accordingly, the level of the positive regulator of virulence, VirF, is much lower in the mutant than in the wild type. However, the transcription of the virF gene in minimal medium is the same in the wild type and in the tgt mutant. As the undermodification of tRNA is not affected by the quality of the growth medium, we conclude that such an environmental change in growth conditions partly restores virulence gene expression by counteracting poor translation of the virF mRNA mediated by an oQ-deficient tRNA. Virulence gene expression is partly restored in the tgt mutant by the addition of a mixture of arginine and methionine. Addition of the polyamine putrescine, synthesis of which is metabolically related to that of arginine and methionine, has a comparable stimulatory effect on virulence gene expression. These results not only suggest a role for amino acids and polyamines in the environmental regulation of virulence gene expression in S. flexneri , but also demonstrate a strong and specific involvement of tRNA modifications, and especially oQ, in the adaptation of virulence gene expression to the nutritional quality of the growth medium.

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A Chromosomal Locus Which Controls the Ability of Shigella flexneri to Evoke Keratoconjunctivitis

Cited by 105 publications

References 13 publications

Molecular epidemiology of plasmid patterns inShigella flexneritypes 1–6

Molecular epidemiology of plasmid patterns inShigella flexneritypes 1–6

Black holes, antivirulence genes, and gene inactivation in the evolution of bacterial pathogens

Putrescine or a combination of methionine and arginine restores virulence gene expression in a tRNA modification‐deficient mutant of Shigella flexneri: a possible role in adaptation of virulence

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