Genome-wide transcriptional response of an avian pathogenic Escherichia coli (APEC) pst mutant

Crépin, Sébastien; Lamarche, Martin G.; Garneau, Philippe; Séguin, Julie; Proulx, Julie; Dozois, Charles M.; Harel, Josée

doi:10.1186/1471-2164-9-568

Cited by 33 publications

(55 citation statements)

References 68 publications

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“…Briefly, 4 g/ml of p-nitrophenyl phosphate was added to 500 l of mid-log-phase (optical density at 600 nm [OD 600 ] of 0.6) culture cells Sensitivity of E. coli strains to hydrogen peroxide. Sensitivity to hydrogen peroxide-induced oxidative stress was determined by an agar overlay diffusion method on LB or LP plates (1.5% agar) as described previously (3,43), with some modifications (10). Overnight cultures grown in LB or LP broth were adjusted to an OD 600 of 0.5.…”

Section: Methodsmentioning

confidence: 99%

“…Transcriptional analyses demonstrated the induction of a general stress response in the pst mutant, including increased expression of genes involved in adaptation to acid stress, oxidative stress, and the general stress response (notably RpoS-regulated genes). In addition, genes associated with cell surface composition were modulated (10). Since the Pst system contributes both to regulation of the Pho regulon and to high-affinity uptake of P i , it remains to be determined if the effects of Pst inactivation on APEC virulence are mediated through the PhoBR TCRS or deficiency in phosphate uptake (28).…”

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confidence: 99%

“…Furthermore, it is well recognized that inactivation of the Pst system, constitutive expression of the Pho regulon, and bacterial virulence are linked in diverse bacterial species (28). In APEC strain 7122, deletion of the pstCAB genes was shown to reduce virulence in a chicken infection model and to affect multiple virulence attributes, including production of type 1 fimbriae and resistance to cationic peptides, to the bactericidal effects of rabbit serum, to acid shock, and to oxidative stress (10,26). Transcriptional analyses demonstrated the induction of a general stress response in the pst mutant, including increased expression of genes involved in adaptation to acid stress, oxidative stress, and the general stress response (notably RpoS-regulated genes).…”

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Increased Pho Regulon Activation Correlates with Decreased Virulence of an Avian Pathogenic Escherichia coli O78 Strain

et al. 2010

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Avian pathogenic Escherichia coli (APEC) strains are associated with respiratory infections, septicemia, cellulitis, peritonitis, and other conditions, since colibacillosis manifests in many ways. The Pho regulon is jointly controlled by the two-component regulatory system PhoBR and by the phosphate-specific transport (Pst) system. To determine the specific roles of the PhoBR regulon and the Pst system in the pathogenesis of the APEC O78 strain 7122, different phoBR and pst mutant strains were tested in vivo in chickens and in vitro for virulence traits. Mutations resulting in constitutive activation of the Pho regulon rendered strains more sensitive than the wild type to hydrogen peroxide and to the bactericidal effects of rabbit serum. In addition, production of type 1 fimbriae was also impaired in these strains. Using a chicken competitive infection model, all PhoB constitutive mutants were outcompeted by the wild-type parent, including strains containing a functional Pst system. Cumulative inactivation of the Pst system and the PhoB regulator resulted in a restoration of virulence. In addition, loss of the PhoB regulator alone did not affect virulence in the chicken infection model. Interestingly, the level of attenuation of the mutant strains correlated directly with the level of activation of the Pho regulon. Overall, results indicate that activation of the Pho regulon rather than phosphate transport by the Pst system plays a major role in the attenuation of the APEC O78 strain 7122.

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Section: Methodsmentioning

confidence: 99%

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confidence: 99%

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Increased Pho Regulon Activation Correlates with Decreased Virulence of an Avian Pathogenic Escherichia coli O78 Strain

et al. 2010

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“…Flagellin contributes to persistence and invasion after oral dosing of chicks with APEC O78 (28), and ExPEC invasins (Ibe proteins) also facilitate APEC invasion (35,36). Indirect effects on the expression of virulence-associated fimbriae have been reported for mutants with a constitutively activated pho regulon (37) and those lacking the pst system (38), ibeA, ibeB, and ibeT (36,39), the barA-uvrY-encoded two-component sensory system (40), and a type VI protein secretion system (41). These reports may partially explain the attenuation of such mutants in chickens and indicate that the effect of mutations may propagate through complex networks.…”

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Sequencing and Functional Annotation of Avian Pathogenic Escherichia coli Serogroup O78 Strains Reveal the Evolution of E. coli Lineages Pathogenic for Poultry via Distinct Mechanisms

et al. 2013

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f Avian pathogenic Escherichia coli (APEC) causes respiratory and systemic disease in poultry. Sequencing of a multilocus sequence type 95 (ST95) serogroup O1 strain previously indicated that APEC resembles E. coli causing extraintestinal human diseases. We sequenced the genomes of two strains of another dominant APEC lineage (ST23 serogroup O78 strains 7122 and IMT2125) and compared them to each other and to the reannotated APEC O1 sequence. For comparison, we also sequenced a human enterotoxigenic E. coli (ETEC) strain of the same ST23 serogroup O78 lineage. Phylogenetic analysis indicated that the APEC O78 strains were more closely related to human ST23 ETEC than to APEC O1, indicating that separation of pathotypes on the basis of their extraintestinal or diarrheagenic nature is not supported by their phylogeny. The accessory genome of APEC ST23 strains exhibited limited conservation of APEC O1 genomic islands and a distinct repertoire of virulence-associated loci. In light of this diversity, we surveyed the phenotype of 2,185 signature-tagged transposon mutants of 7122 following intra-air sac inoculation of turkeys. This procedure identified novel APEC ST23 genes that play strain-and tissue-specific roles during infection. For example, genes mediating group 4 capsule synthesis were required for the virulence of 7122 and were conserved in IMT2125 but absent from APEC O1. Our data reveal the genetic diversity of E. coli strains adapted to cause the same avian disease and indicate that the core genome of the ST23 lineage serves as a chassis for the evolution of E. coli strains adapted to cause avian or human disease via acquisition of distinct virulence genes. Avian pathogenic Escherichia coli (APEC) imposes substantial economic and welfare costs on poultry producers worldwide. Respiratory infections typically involve inflammation of the air sacs and lung and may spread to visceral organs, causing perihepatitis, pericarditis, peritonitis, salpingitis, and sepsis (1). A need exists for effective cross-protective vaccines to control APEC in poultry, since autologous bacterins confer limited serotype-specific protection, and control via antibiotics is hindered by resistance and restrictions on prophylaxis. Diverse serotypes are associated with disease, and the molecular mechanisms underlying mucosal colonization and systemic translocation are ill defined. Serogroup O1, O2, and O78 strains are frequently isolated from diseased poultry and mostly belong to multilocus sequence types 95 and 23 (ST95 and ST23) (http://mlst.ucc.ie/mlst/dbs/Ecoli), as evidenced by recent surveys in chickens (2) and turkeys (3). The genetic traits that define the APEC pathotype and the extent of inter-and intra-ST and serogroup diversity are incompletely understood.Sequencing of the complete genome of a ST95 strain of APEC serotype O1:K1:H7 (APEC O1) revealed that it is closely related to extraintestinal pathogenic E. coli (ExPEC) strains associated with human urinary tract infections (4). This is further evident from multilocus sequence ...

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“…Whereas various virulence factors of ExPEC strains of avian origin were described, these factors, present in various combinations among strains, cannot completely explain the entire pathogenicity mechanism, which is complex and multifactorial (10,11,13,14,19,24,26,36,37,49,53). To improve our knowledge in that domain and identify new virulence factors, a subtractive hybridization between the genomes of the avian ExPEC strain MT512 (02:K1:H7) and of the avirulent avian strain EC79 (O2:K Ϫ :H Ϫ ) was performed in our laboratory.…”

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A Metabolic Operon in Extraintestinal PathogenicEscherichia coliPromotes Fitness under Stressful Conditions and Invasion of Eukaryotic Cells

et al. 2009

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We identified a carbohydrate metabolic operon (frz) that is highly associated with extraintestinal pathogenic Escherichia coli (ExPEC) strains. The frz operon codes for three subunits of a phosphoenolpyruvate:carbohydrate phosphotransferase system (PTS) transporter of the fructose subfamily, for a transcriptional activator of PTSs of the MgA family, for two type II ketose-1,6-bisphosphate aldolases, for a sugar-specific kinase (repressor, open reading frame, kinase family [ROK]), and for a protein of the cupin superfamily. We proved that the frz operon promotes bacterial fitness under stressful conditions, such as oxygen restriction, late stationary phase of growth, or growth in serum or in the intestinal tract. Furthermore, we showed that frz is involved in adherence to and internalization in human type II pneumocytes, human enterocytes, and chicken liver cells by favoring the ON orientation of the fim operon promoter and thus acting on the expression of type 1 fimbriae, which are the major ExPEC adhesins. Both the PTS activator and the metabolic enzymes encoded by the frz operon are involved in these phenotypes.

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Genome-wide transcriptional response of an avian pathogenic Escherichia coli (APEC) pst mutant

Cited by 33 publications

References 68 publications

Increased Pho Regulon Activation Correlates with Decreased Virulence of an Avian Pathogenic Escherichia coli O78 Strain

Increased Pho Regulon Activation Correlates with Decreased Virulence of an Avian Pathogenic Escherichia coli O78 Strain

Sequencing and Functional Annotation of Avian Pathogenic Escherichia coli Serogroup O78 Strains Reveal the Evolution of E. coli Lineages Pathogenic for Poultry via Distinct Mechanisms

A Metabolic Operon in Extraintestinal PathogenicEscherichia coliPromotes Fitness under Stressful Conditions and Invasion of Eukaryotic Cells

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