scholarly journals Excision of the Shigella Resistance Locus Pathogenicity Island in Shigella flexneri Is Stimulated by a Member of a New Subgroup of Recombination Directionality Factors

2004 ◽  
Vol 186 (16) ◽  
pp. 5551-5554 ◽  
Author(s):  
Shelley N. Luck ◽  
Sally A. Turner ◽  
Kumar Rajakumar ◽  
Ben Adler ◽  
Harry Sakellaris
Keyword(s):  
Escherichia Coli ◽  
Sequence Analysis ◽  
Yersinia Pestis ◽  
Shigella Flexneri ◽  
Pathogenicity Island ◽  
Pathogenicity Islands ◽  
Resistance Locus ◽  
Bacterial Chromosomes

ABSTRACT Pathogenicity islands are capable of excision and insertion within bacterial chromosomes. We describe a protein, Rox, that stimulates excision of the Shigella resistance locus pathogenicity island in Shigella flexneri. Sequence analysis suggests that Rox belongs to a new subfamily of recombination directionality factors, which includes proteins from P4, enterohemorrhagic Escherichia coli, and Yersinia pestis.

scholarly journals Role of attP in Integrase-Mediated Integration of the Shigella Resistance Locus Pathogenicity Island of Shigella flexneri

2004 ◽  
Vol 48 (3) ◽  
pp. 1028-1031 ◽  
Author(s):  
Sally A. Turner ◽  
Shelley N. Luck ◽  
Harry Sakellaris ◽  
Kumar Rajakumar ◽  
Ben Adler
Keyword(s):  
Shigella Flexneri ◽  
Pathogenicity Island ◽  
Resistance Locus ◽  
Site Specific ◽  
Site Specific Recombination ◽  
Independent Site

ABSTRACT The Shigella resistance locus (SRL) pathogenicity island (PAI) in Shigella spp. mediates resistance to streptomycin, ampicillin, chloramphenicol, and tetracycline. It can be excised from the chromosome via site-specific recombination mediated by the P4-related int gene. Here, we show that SRL PAI attP is capable of RecA-independent, site-specific, int-mediated integration into two bacterial tRNA attB sites.

scholarly journals Nested Deletions of the SRL Pathogenicity Island ofShigella flexneri 2a

2001 ◽  
Vol 183 (19) ◽  
pp. 5535-5543 ◽  
Author(s):  
Sally A. Turner ◽  
Shelley N. Luck ◽  
Harry Sakellaris ◽  
Kumar Rajakumar ◽  
Ben Adler
Keyword(s):  
Sequence Data ◽  
Shigella Flexneri ◽  
Tetracycline Resistance ◽  
Pathogenicity Island ◽  
Resistance Locus ◽  
Integrase Gene ◽  
Chromosomal Site ◽  
In The Wild ◽  
Selection For ◽  
Nested Deletions

ABSTRACT In this study, we determined the boundaries of a 99-kb deletable element of Shigella flexneri 2a strain YSH6000. The element, designated the multiple-antibiotic resistance deletable element (MRDE), had recently been found to contain a 66-kb pathogenicity island (PAI)-like element (designated the SRL PAI) which carries the Shigella resistance locus (SRL), encoding resistance determinants to streptomycin, ampicillin, chloramphenicol, and tetracycline. The YSH6000 MRDE was found to be flanked by two identical IS91 elements present at the S. flexneri homologs of the Escherichia coli genesputA and mdoA on NotI fragment D. Sequence data from two YSH6000-derived MRDE deletants, YSH6000T and S2430, revealed that deletion of the MRDE occurred between the two flanking IS91 elements, resulting in a single IS91 element spanning the two original IS91 loci. Selection for the loss of tetracycline resistance confirmed that the MRDE deletion occurred reproducibly from the same chromosomal site and also showed that the SRL PAI and the SRL itself were capable of independent deletion from the chromosome, thus revealing a unique set of nested deletions. The excision frequency of the SRL PAI was estimated to be 10−5 per cell in the wild type, and mutation of a P4-like integrase gene (int) at the left end of the SRL PAI revealed that int mediates precise deletion of the PAI.

scholarly journals The shdA Gene Is Restricted to Serotypes ofSalmonella enterica Subspecies I and Contributes to Efficient and Prolonged Fecal Shedding

2000 ◽  
Vol 68 (5) ◽  
pp. 2720-2727 ◽  
Author(s):  
Robert A. Kingsley ◽  
Karin van Amsterdam ◽  
Naomi Kramer ◽  
Andreas J. Bäumler
Keyword(s):  
Escherichia Coli ◽  
Amino Acid ◽  
Sequence Analysis ◽  
Amino Acid Sequence ◽  
Domestic Fowl ◽  
Shigella Flexneri ◽  
Open Reading Frame ◽  
Fecal Shedding ◽  
Reading Frame ◽  
K 12

ABSTRACT Little is known about factors which enable Salmonellaserotypes to circulate within populations of livestock and domestic fowl. We have identified a DNA region which is present inSalmonella serotypes commonly isolated from livestock and domestic fowl (S. enterica subspecies I) but absent from reptile-associated Salmonella serotypes (S. bongori and S. enterica subspecies II to VII). This DNA region was cloned from Salmonella serotype Typhimurium and sequence analysis revealed the presence of a 6,105-bp open reading frame, designated shdA, whose product's deduced amino acid sequence displayed homology to that of AIDA-I from diarrheagenicEscherichia coli, MisL of serotype Typhimurium, and IcsA ofShigella flexneri. The shdA gene was located adjacent to xseA at 52 min, in a 30-kb DNA region which is not present in Escherichia coli K-12. A serotype Typhimurium shdA mutant was shed with the feces in reduced numbers and for a shorter period of time compared to its isogenic parent. A possible role for the shdA gene during the expansion in host range of S. enterica subspecies I to include warm-blooded vertebrates is discussed.

scholarly journals Uropathogenic Escherichia coli Suppresses the Host Inflammatory Response via Pathogenicity Island Genes sisA and sisB

2009 ◽  
Vol 77 (12) ◽  
pp. 5322-5333 ◽  
Author(s):  
Amanda L. Lloyd ◽  
Sara N. Smith ◽  
Kathryn A. Eaton ◽  
Harry L. T. Mobley
Keyword(s):  
Escherichia Coli ◽  
Immune Response ◽  
Urinary Tract ◽  
Inflammatory Response ◽  
Shigella Flexneri ◽  
Pathogenicity Island ◽  
Host Immune Response ◽  
Wild Type ◽  
Host Inflammatory Response

ABSTRACT Extraintestinal pathogenic Escherichia coli can successfully colonize the urinary tract of the immunocompetent host. In part, this is accomplished by dampening the host immune response. Indeed, the sisA and sisB genes (shiA-like inflammation suppressor genes A and B) of uropathogenic E. coli strain CFT073, homologs of the Shigella flexneri SHI-2 pathogenicity island gene shiA, suppress the host inflammatory response. A double deletion mutant (ΔsisA ΔsisB) resulted in a hyperinflammatory phenotype in an experimental model of ascending urinary tract infection. The ΔsisA ΔsisB mutant not only caused significantly more inflammatory foci in the kidneys of CBA/J mice (P = 0.0399), but these lesions were also histologically more severe (P = 0.0477) than lesions observed in mice infected with wild-type CFT073. This hyperinflammatory phenotype could be suppressed to wild-type levels by in vivo complementation of the ΔsisA ΔsisB mutant with either the sisA or sisB gene in trans. The ΔsisA ΔsisB mutant was outcompeted by wild-type CFT073 during cochallenge infection in the bladder (P = 0.0295) at 48 h postinoculation (hpi). However, during cochallenge infections, we reasoned that wild-type CFT073 could partially complement the ΔsisA ΔsisB mutant. Consistent with this, the most significant colonization defect of the ΔsisA ΔsisB mutant in vivo was observed during independent challenge relative to wild-type CFT073, with attenuation of the mutant observed in the bladder (P < 0.0001) and kidneys (P = 0.0003) at 6 hpi. By 24 and 48 hpi, the ΔsisA ΔsisB mutant was no longer significantly attenuated in the bladder or kidneys, suggesting that the sisA and sisB genes may be important for suppressing the host immune response during the initial stages of infection.

scholarly journals Distribution of Pathogenicity Islands OI-122, OI-43/48, and OI-57 and a High-Pathogenicity Island in Shiga Toxin-Producing Escherichia coli

2013 ◽  
Vol 79 (11) ◽  
pp. 3406-3412 ◽  
Author(s):  
Wenting Ju ◽  
Jinling Shen ◽  
Magaly Toro ◽  
Shaohua Zhao ◽  
Jianghong Meng
Keyword(s):  
Escherichia Coli ◽  
Shiga Toxin ◽  
Phylogenetic Trees ◽  
Virulence Genes ◽  
Severe Disease ◽  
Strong Association ◽  
Pathogenicity Island ◽  
Pathogenicity Islands ◽  
Content Type ◽  
High Pathogenicity

ABSTRACTPathogenicity islands (PAIs) play an important role in Shiga toxin-producingEscherichia coli(STEC) pathogenicity. The distribution of PAIs OI-122, OI-43/48, and OI-57 and a high-pathogenicity island (HPI) were determined among 98 STEC strains assigned to seropathotypes (SPTs) A to E. PCR and PCR-restriction fragment length polymorphism assays were used to identify 14 virulence genes that belonged to the four PAIs and to subtypeeaeandstxgenes, respectively. Phylogenetic trees were constructed based on the sequences ofpagCamong 34 STEC strains andihaamong 67 diverse pathogenicE. coli, respectively. Statistical analysis demonstrated that the prevalences of OI-122 (55.82%) and OI-57 (82.35%) were significantly greater in SPTs (i.e., SPTs A, B, and C) that are frequently associated with severe disease than in other SPTs.terC(62.5%) andureC(62.5%) in OI-43/48 were also significantly more prevalent in SPTs A, B, and C than in SPTs D and E. In addition, OI-122, OI-57, and OI-43/48 and their associated virulence genes (exceptiha) were found to be primarily associated witheae-positive STEC, whereas HPI occurred independently of theeaepresence. The strong association of OI-122, OI-43/48, and OI-57 witheae-positive STEC suggests in part that different pathogenic mechanisms exist betweeneae-positive andeae-negative STEC strains. Virulence genes in PAIs that are associated with severe diseases can be used as potential markers to aid in identifying highly virulent STEC.

scholarly journals The sigA Gene Which Is Borne on the shePathogenicity Island of Shigella flexneri 2a Encodes an Exported Cytopathic Protease Involved in Intestinal Fluid Accumulation

2000 ◽  
Vol 68 (5) ◽  
pp. 2457-2463 ◽  
Author(s):  
Keith Al-Hasani ◽  
Ian R. Henderson ◽  
Harry Sakellaris ◽  
Kumar Rajakumar ◽  
Travis Grant ◽  
...  
Keyword(s):  
Functional Analysis ◽  
Sequence Analysis ◽  
Serine Protease ◽  
Shigella Flexneri ◽  
Pathogenicity Island ◽  
Intestinal Fluid ◽  
Fluid Accumulation ◽  
Shigella Flexneri 2A ◽  
A Cell ◽  
Processed Form

ABSTRACT In this study, the sigA gene situated on theshe pathogenicity island of Shigella flexneri2a was cloned and characterized. Sequence analysis showed thatsigA encodes a 139.6-kDa protein which belongs to the SPATE (serine protease autotransporters of Enterobacteriaceae) subfamily of autotransporter proteins. The demonstration that SigA is autonomously secreted from the cell to yield a 103-kDa processed form and possesses a conserved C-terminal domain for export from the cell were consistent with the autotransporter pathway of secretion. Functional analysis showed that SigA is a secreted temperature-regulated serine protease capable of degrading casein. SigA was cytopathic for HEp-2 cells, suggesting that it may be a cell-altering toxin with a role in the pathogenesis ofShigella infections. SigA was at least partly responsible for the ability of S. flexneri to stimulate fluid accumulation in ligated rabbit ileal loops.

scholarly journals Molecular Epidemiology of the SRL Pathogenicity Island

2003 ◽  
Vol 47 (2) ◽  
pp. 727-734 ◽  
Author(s):  
Sally A. Turner ◽  
Shelley N. Luck ◽  
Harry Sakellaris ◽  
Kumar Rajakumar ◽  
Ben Adler
Keyword(s):  
Antibiotic Resistance ◽  
Molecular Epidemiology ◽  
Structural Variation ◽  
Shigella Flexneri ◽  
Pathogenicity Island ◽  
Enteric Pathogens ◽  
The Other ◽  
Resistance Locus ◽  
Multiple Antibiotic Resistance ◽  
Linkage Studies

ABSTRACT The Shigella resistance locus (SRL), which is carried on the SRL pathogenicity island (PAI) in Shigella flexneri 2a YSH6000, mediates resistance to the antibiotics streptomycin, ampicillin, chloramphenicol, and tetracycline. In the present study, we investigated the distribution and structural variation of the SRL and the SRL PAI in 71 Shigella isolates and 28 other enteric pathogens by PCR and Southern analysis. The SRL and SRL-related loci, although absent from the other enteric pathogens evaluated in this study, were found to be present in a number of Shigella isolates. SRL PAI markers were also present in the majority of strains carrying the SRL and SRL-related loci. PCR linkage studies with six of these strains demonstrated that the SRL is carried on elements similar in structure and organization to the YSH6000 SRL PAI, consistent with the hypothesis that the SRL PAI may be involved in the spread of multiple-antibiotic resistance in these strains.

scholarly journals The Cloned Locus of Enterocyte Effacement from EnterohemorrhagicEscherichia coli O157:H7 Is Unable To Confer the Attaching and Effacing Phenotype upon E. coliK-12

1999 ◽  
Vol 67 (8) ◽  
pp. 4260-4263 ◽  
Author(s):  
Simon J. Elliott ◽  
Jie Yu ◽  
James B. Kaper
Keyword(s):  
Escherichia Coli ◽  
Pathogenicity Island ◽  
Pathogenicity Islands ◽  
E Coli ◽  
Enterocyte Effacement ◽  
K 12

ABSTRACT The locus of enterocyte effacement (LEE) pathogenicity island of enterohemorrhagic Escherichia coli (EHEC) O157:H7 possesses the same genes in identical order and orientation as the LEE of enteropathogenic E. coli (EPEC) O127:H6 but is unable to form attaching and effacing (A/E) lesions or to secrete Esp proteins when it is cloned in an E. coli K-12 background. The A/E phenotype could not be restored by trans complementation with a variety of cloned EPEC LEE fragments, suggesting functional and/or regulatory differences between the LEE pathogenicity islands of EPEC O127:H6 and EHEC O157:H7.

scholarly journals Serotype 1a O-Antigen Modification: Molecular Characterization of the Genes Involved and Their Novel Organization in the Shigella flexneriChromosome

1999 ◽  
Vol 181 (15) ◽  
pp. 4711-4718 ◽  
Author(s):  
Pradip Adhikari ◽  
Gwen Allison ◽  
Belinda Whittle ◽  
Naresh K. Verma
Keyword(s):  
Sequence Analysis ◽  
Molecular Characterization ◽  
Insertion Sequence ◽  
Shigella Flexneri ◽  
Pathogenicity Islands ◽  
Is Elements ◽  
O Antigen ◽  
Phage Dna

ABSTRACT The factors responsible for serotype 1a O-antigen modification inShigella flexneri were localized to a 5.8-kb chromosomalHindIII fragment of serotype 1a strain Y53. The entire 5.8-kb fragment and regions up- and downstream of it (10.6-kb total) were sequenced. A putative three-gene operon, which showed homology with other serotype conversion genes, was identified and shown to confer serotype 1a O-antigen modification. The serotype conversion genes were flanked on either side by phage DNA. Multiple insertion sequence (IS) elements were located within and upstream of the phage DNA in a composite transposon-like structure. Host DNA homologous to the dsdC and the thrW proA genes was located upstream of the IS elements and downstream of the phage DNA, respectively. The sequence analysis indicates that the organization of the 10.6-kb region of the Y53 chromosome is unique and suggests that the serotype conversion genes were originally brought into the host by a bacteriophage. Several features of this region are also characteristic of pathogenicity islands.

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