Comparative genome mapping with mobile physical map landmarks

Bloch, Craig A.; Rode, Christopher K.; Obreque, Victor; Russell, Kelly Y.

doi:10.1128/jb.176.22.7121-7125.1994

Cited by 14 publications

(13 citation statements)

References 29 publications

(11 reference statements)

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“…Nevertheless, they do suggest the possibility of numerous additional targets for protective interventions if a virulence role for any of these traits in NBM can be confirmed in vivo. The results of subtractive hybridization analysis of NBM isolate C5 [55,56] and of genome mapping of strain RS218 [57,68], together with the high prevalence of PAI marker malX noted here, suggest that numerous additional VFs await discovery within the PAIs of NBMderived E. coli.…”

Section: Figurementioning

confidence: 82%

Phylogenetic Distribution of Virulence‐Associated Genes amongEscherichia coliIsolates Associated with Neonatal Bacterial Meningitis in The Netherlands

et al. 2002

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Seventy cerebrospinal fluid Escherichia coli isolates from infants with neonatal bacterial meningitis (NBM), as submitted to the Netherlands Reference Laboratory for Bacterial Meningitis from 1989 through 1997, were assessed for phylogenetic background and extended virulence genotypes, in comparison with the E. coli reference collection, by using molecular methods. Phylogenetic group B2 significantly predominated overall (81%). The 4 major phylogenetic clusters exhibited distinctive virulence genotypes, suggesting diverse evolutionary histories for the individual genes. Many genes not previously studied in NBM, notably diarrhea-associated cdtB (cytolethal distending toxin [46%]) and urinary tract infection-associated ompT (outer membrane protease T [96%]), were as or more prevalent than traditional NBM-associated traits, such as ibeA (invasion of brain endothelium [33%]), sfaS (S fimbriae [59%]), and K1 capsule (81%). These findings provide novel insights into the phylogenetic origins of NBM-associated E. coli and suggest numerous new potential targets for preventive interventions against this dire disease.

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Section: Figurementioning

confidence: 82%

Phylogenetic Distribution of Virulence‐Associated Genes amongEscherichia coliIsolates Associated with Neonatal Bacterial Meningitis in The Netherlands

et al. 2002

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“…E. coli MG1655 mutants containing Tn10dSpcRCP2 or Tn10dCamRCP2 insertions were generated by electroporation with plasmids pGI300 or pGI310 as described (14). MG1655 double insertion mutants and single and double insertion mutants of S. flexneri 2a strain BS103 were generated by transducing recipient strains with P1⌬dam rev6 lysates of MG1655 insertion mutants (15).…”

mentioning

confidence: 99%

“Black holes” and bacterial pathogenicity: A large genomic deletion that enhances the virulence of Shigella spp. and enteroinvasive Escherichia coli

Maurelli

Fernández²,

Bloch³

et al. 1998

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

407

308

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Plasmids, bacteriophages, and pathogenicity islands are genomic additions that contribute to the evolution of bacterial pathogens. For example, Shigella spp., the causative agents of bacillary dysentery, differ from the closely related commensal Escherichia coli in the presence of a plasmid in Shigella that encodes virulence functions. However, pathogenic bacteria also may lack properties that are characteristic of nonpathogens. Lysine decarboxylase (LDC) activity is present in Ϸ90% of E. coli strains but is uniformly absent in Shigella strains. When the gene for LDC, cadA, was introduced into Shigella flexneri 2a, virulence became attenuated, and enterotoxin activity was inhibited greatly. The enterotoxin inhibitor was identified as cadaverine, a product of the reaction catalyzed by LDC. Comparison of the S. flexneri 2a and laboratory E. coli K-12 genomes in the region of cadA revealed a large deletion in Shigella. Representative strains of Shigella spp. and enteroinvasive E. coli displayed similar deletions of cadA. Our results suggest that, as Shigella spp. evolved from E. coli to become pathogens, they not only acquired virulence genes on a plasmid but also shed genes via deletions. The formation of these ''black holes,'' deletions of genes that are detrimental to a pathogenic lifestyle, provides an evolutionary pathway that enables a pathogen to enhance virulence. Furthermore, the demonstration that cadaverine can inhibit enterotoxin activity may lead to more general models about toxin activity or entry into cells and suggests an avenue for antitoxin therapy. Thus, understanding the role of black holes in pathogen evolution may yield clues to new treatments of infectious diseases.

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“…Whole genomes have been analyzed in the manner traditionally available only for plasmid-sized DNAs, allowing strains to be characterized (i) by physical mapping for the analysis of genomic organization and gene locus relationships (4,6,8,31,37), (ii) through genomic macrorestriction fingerprinting for population analysis and epidemiologic studies (36), (iii) through intraand interspecies comparative genomics (9,37), and (iv) by nucleotide sequence after fragmentation of the genome into contiguous and/or nonoverlapping segments (5,7,30). Ultimately, a macrorestriction map from a given strain integrated with the species' genetic map may provide a critical step in studying that strain's uniqueness.…”

Section: Discussionmentioning

confidence: 99%

“…Eight different insertions that contributed to physical mapping were found to also cause J96 auxotrophies that, by a combination of auxanography and map location, could be inferred to interrupt homologs of genes previously described for strain K-12. Thus, these insertions allowed integration of the newly constructed (and largely featureless) J96 physical map with the extensively characterized E. coli genetic map (9).…”

Section: Vol 68 2000mentioning

confidence: 99%

“…Six of these eight virulence genes were found, as expected, at sequences corresponding to the locations of either of the two J96 pathogenicity islands Pai-4 (also called Pai-I) and Pai-5 (also called Pai-II). These pathogenic polymorphisms have been detected by the crossing of Tn10dRCP2 alleles between strains K-12 and J96 to allow alignment of their chromosomes' physical maps into heteroduplex-like structures (9). Also, the foc genes, encoding F1C pili, were mapped to 25 min (35,40), the same region containing the related sfa genes in newborn sepsis-associated E. coli (37).…”

Section: Vol 68 2000mentioning

confidence: 99%

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Integrated Genomic Map from Uropathogenic Escherichia coli J96

Melkerson-Watson¹,

Rode²,

Zhang

et al. 2000

Infect Immun

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Escherichia coli J96 is a uropathogen having both broad similarities to and striking differences from nonpathogenic, laboratory E. coli K-12. Strain J96 contains three large (>100-kb) unique genomic segments integrated on the chromosome; two are recognized as pathogenicity islands containing urovirulence genes. Additionally, the strain possesses a fourth smaller accessory segment of 28 kb and two deletions relative to strain K-12. We report an integrated physical and genetic map of the 5,120-kb J96 genome. The chromosome contains 26 NotI, 13 BlnI, and 7 I-CeuI macrorestriction sites. Macrorestriction mapping was rapidly accomplished by a novel transposon-based procedure: analysis of modified minitransposon insertions served to align the overlapping macrorestriction fragments generated by three different enzymes (each sharing a common cleavage site within the insert), thus integrating the three different digestion patterns and ordering the fragments. The resulting map, generated from a total of 54 mini-Tn10 insertions, was supplemented with auxanography and Southern analysis to indicate the positions of insertionally disrupted aminosynthetic genes and cloned virulence genes, respectively. Thus, it contains not only physical, macrorestriction landmarks but also the loci for eight housekeeping genes shared with strain K-12 and eight acknowledged urovirulence genes; the latter confirmed clustering of virulence genes at the large unique accessory chromosomal segments. The 115-kb J96 plasmid was resolved by pulsed-field gel electrophoresis in NotI digests. However, because the plasmid lacks restriction sites for the enzymes BlnI and I-CeuI, it was visualized in BlnI and I-CeuI digests only of derivatives carrying plasmid inserts artificially introducing these sites. Owing to an I-SceI site on the transposon, the plasmid could also be visualized and sized from plasmid insertion mutants after digestion with this enzyme. The insertional strains generated in construction of the integrated genomic map provide useful physical and genetic markers for further characterization of the J96 genome.

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Comparative genome mapping with mobile physical map landmarks

Abstract: We describe a method for comparative macrorestriction mapping of the chromosomes of Escherichia coli strains. In this method, a series of physically tagged E. coli K-12

Cited by 14 publications

References 29 publications

Phylogenetic Distribution of Virulence‐Associated Genes amongEscherichia coliIsolates Associated with Neonatal Bacterial Meningitis in The Netherlands

Phylogenetic Distribution of Virulence‐Associated Genes amongEscherichia coliIsolates Associated with Neonatal Bacterial Meningitis in The Netherlands

“Black holes” and bacterial pathogenicity: A large genomic deletion that enhances the virulence of Shigella spp. and enteroinvasive Escherichia coli

Integrated Genomic Map from Uropathogenic Escherichia coli J96

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