Type-Specific Contributions to Chromosome Size Differences in
            <i>Escherichia coli</i>

Rode, Christopher K.; Melkerson-Watson, L.J.; Johnson, Amanda T.; Bloch, Craig A.

doi:10.1128/iai.67.1.230-236.1999

Cited by 70 publications

(21 citation statements)

References 44 publications

(45 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Identi¢cation of puvA validates the hypothesis that novel genes are required for invasive disease by E. coli K1. It remains to be determined whether puvA or other puv genes isolated in the future will map to any of the six to 12 K1-speci¢c regions of the genome previously identi¢ed by macrorestriction or subtractive hybridization techniques [13,14].…”

Section: Identi¢cation Of Systemic Virulence Genes By Dna Sequence Anmentioning

confidence: 99%

Adaptation of signature-tagged mutagenesis to Escherichia coli K1 and the infant-rat model of invasive disease

González

2001

FEMS Microbiology Letters

View full text Add to dashboard Cite

With the exception of the polysialic acid capsule (K1 antigen), little is known about other virulence factors needed for systemic infection by Escherichia coli K1, the leading cause of Gram-negative neonatal meningitis in humans. In this work, the functional genomics method of signature-tagged mutagenesis (STM) was adapted to E. coli K1 and the infant-rat model to identify non-capsule virulence genes. Validation of the method was demonstrated by the failure to recover a reconstructed acapsular mutant from bacterial pools used to systemically infect 5-day-old rats. Three new genes required for systemic disease were identified from a total of 192 mutants screened by STM (1.56% hit rate). Gut colonization, Southern blot hybridization, mixed-challenge infection, and DNA sequence analyses showed that the attenuating defects in the mutants were associated with transposon insertions in rfaL (O antigen ligase), dsbA (thiol:disulfide oxidoreductase), and a new gene, puvA (previously unidentified virulence gene A), with no known homologues. The results indicate the ability of STM to identify novel systemic virulence factors in E. coli K1. ß 2001 Published by Elsevier Science B.V. on behalf of the Federation of European Microbiological Societies.

show abstract

Section: Identi¢cation Of Systemic Virulence Genes By Dna Sequence Anmentioning

confidence: 99%

Adaptation of signature-tagged mutagenesis to Escherichia coli K1 and the infant-rat model of invasive disease

González

2001

FEMS Microbiology Letters

View full text Add to dashboard Cite

show abstract

“…The genome size of naturally occurring E. coli isolates can differ by up to 1 Mb, ranging from approximately 4.5 to 5.5 Mb (5). This variability is reflected in the commensal E. coli K-12 isolate MG1655 (4.64 Mb) (9), the enterohemorrhagic E. coli (EHEC) strains O157:H7 Sakai (5.50 Mb) (38) and O157:H7 EDL933 (5.53 Mb) (77), the enteroaggregative E. coli (EAEC) strain O42 (5.36 Mb) (www.sanger.ac.uk), and UPEC isolates CFT073 (5.23 Mb) (104), J96 (5.06 Mb) (83), 536 (4.94 Mb) (16), and UTI89 (5.07 Mb) (20). The observed differences in genome size between different E. coli strains are primarily due to the insertion or deletion of a few large chromosomal regions, with overall gene order maintained between different strains (83).…”

mentioning

confidence: 99%

Uropathogenic Escherichia coli

Mobley¹,

Donnenberg²,

Hagan³

2009

EcoSal

View full text Add to dashboard Cite

Uropathogenic Escherichia coli (UPEC) strains are responsible for the majority of uncomplicated urinary tract infections, which can present clinically as cystitis or pyelonephritis. UPEC strain CFT073, isolated from the blood of a patient with acute pyelonephritis, was most cytotoxic and most virulent in mice among our strain collection. Based on the genome sequence of CFT073, microarrays were utilized in comparative genomic hybridization (CGH) analysis of a panel of uropathogenic and fecal/commensal E. coli isolates. Genomic DNA from seven UPEC (three pyelonephritis and four cystitis) isolates and three fecal/commensal strains, including K-12 MG1655, was hybridized to the CFT073 microarray. The CFT073 genome contains 5,379 genes; CGH analysis revealed that 2,820 (52.4%) of these genes were common to all 11 E. coli strains, yet only 173 UPEC-specific genes were found by CGH to be present in all UPEC strains but in none of the fecal/commensal strains. When the sequences of three additional sequenced UPEC strains (UTI89, 536, and F11) and a commensal strain (HS) were added to the analysis, 131 genes present in all UPEC strains but in no fecal/commensal strains were identified. Seven previously unrecognized genomic islands (>30 kb) were delineated by CGH in addition to the three known pathogenicity islands. These genomic islands comprise 672 kb of the 5,231-kb (12.8%) genome, demonstrating the importance of horizontal transfer for UPEC and the mosaic structure of the genome. UPEC strains contain a greater number of iron acquisition systems than do fecal/commensal strains, which is reflective of the adaptation to the iron-limiting urinary tract environment. Each strain displayed distinct differences in the number and type of known virulence factors. The large number of hypothetical genes in the CFT073 genome, especially those shown to be UPEC specific, strongly suggests that many urovirulence factors remain uncharacterized.Escherichia coli strains capable of causing disease outside the gastrointestinal tract belong to a diverse group of isolates referred to as extraintestinal pathogenic E. coli (ExPEC) (50, 84). ExPEC strains are responsible for a variety of diseases, including urinary tract infections (UTIs), newborn meningitis, septicemia, nosocomial pneumonia, intra-abdominal infections, osteomyelitis and wound infections (22,27,49,84). Uropathogenic E. coli (UPEC), a prominent member of the ExPEC family, is responsible for up to 90% of uncomplicated UTIs in otherwise healthy individuals (108). An infection occurs primarily by the ascending route following the contamination of the periurethral area, presumably via a fecal reservoir. Bacteria ascend the urethra and colonize the bladder, resulting in cystitis, and in severe cases, infection may spread up the ureters to the kidneys, causing pyelonephritis (15). A serious and potentially life-threatening complication of pyelonephritis occurs when bacteria invade the bloodstream and produce a systemic infection. Due to anatomical differences, UTIs are significantly mo...

show abstract

“…Various techniques, such as macro-restriction analysis, pulsed field gel electrophoresis, genomic subtraction and DNA arrays, have been used successfully with many bacterial species in order to assess their genetic variability (Diatchenko et al, 1996;Rode et al, 1999;Melkerson-Watson et al, 2000;Dorrell et al, 2005). In the present study, SSH between an APEC and an AFEC was run in order to detect genomic differences between pathogenic and nonpathogenic avian E. coli.…”

Section: Discussionmentioning

confidence: 99%

Unique DNA sequences of avian pathogenicEscherichia coliisolates as determined by genomic suppression subtractive hybridization

Kariyawasam¹,

Johnson²,

Nolan³

2006

FEMS Microbiology Letters

View full text Add to dashboard Cite

Genomic suppression subtractive hybridization was carried out between an avian pathogenic Escherichia coli (APEC) and an E. coli isolate from apparently healthy poultry (avian fecal E. coli or AFEC) to understand the genomic differences between APEC and AFEC and to identify potential virulence genes. In an effort to ensure that the genes identified were novel, tester and driver strains were chosen by their similarities in certain known virulence genes. In total, 24 subtractive hybridization fragments specific for APEC were obtained. Eight of the fragments were phage or plasmid related, 13 matched to chromosomal regions and three did not show homology to any known genes. We further determined the association of APEC-specific fragments with virulence by screening a collection of APEC, AFEC and human uropathogenic E. coli (UPEC) using the PCR. Chromosomally located fragments that matched to the ireA iron-responsive element gene, the tia invasion determinant gene, the ibeA invasion gene, genes encoding P pili and a gene encoding aldo/keto reductase were present at significantly higher frequencies in APEC and UPEC than in AFEC, suggesting their contribution to the virulence of extraintestinal pathogenic E. coli. No genes were found to be specific to APEC alone.

show abstract

Type-Specific Contributions to Chromosome Size Differences in Escherichia coli

Cited by 70 publications

References 44 publications

Adaptation of signature-tagged mutagenesis to Escherichia coli K1 and the infant-rat model of invasive disease

Adaptation of signature-tagged mutagenesis to Escherichia coli K1 and the infant-rat model of invasive disease

Uropathogenic Escherichia coli

Unique DNA sequences of avian pathogenicEscherichia coliisolates as determined by genomic suppression subtractive hybridization

Contact Info

Product

Resources

About