Open Access Research article

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

Sébastien Crépin12, Martin G Lamarche12, Philippe Garneau1, Julie Séguin2, Julie Proulx2, Charles M Dozois2 and Josée Harel1*

Author Affiliations

1 Groupe de Recherche sur les Maladies Infectieuses du Porc (GREMIP), Université de Montréal, Faculté de médecine vétérinaire, C. P. 5000, Saint-Hyacinthe, Québec, J2S 7C6, Canada

2 Institut National de la Recherche Scientifique, INRS-Institut Armand-Frappier, Laval, Québec, Canada

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BMC Genomics 2008, 9:568  doi:10.1186/1471-2164-9-568

Published: 28 November 2008

Abstract

Background

Avian pathogenic E. coli (APEC) are associated with extraintestinal diseases in poultry. The pstSCAB-phoU operon belongs to the Pho regulon and encodes the phosphate specific transport (Pst) system. A functional Pst system is required for full virulence in APEC and other bacteria and contributes to resistance of APEC to serum, to cationic antimicrobial peptides and acid shock. The global mechanisms contributing to the attenuation and decreased resistance of the APEC pst mutant to environmental stresses have not been investigated at the transcriptional level. To determine the global effect of a pst mutation on gene expression, we compared the transcriptomes of APEC strain χ7122 and its isogenic pst mutant (K3) grown in phosphate-rich medium.

Results

Overall, 470 genes were differentially expressed by at least 1.5-fold. Interestingly, the pst mutant not only induced systems involved in phosphate acquisition and metabolism, despite phosphate availability, but also modulated stress response mechanisms. Indeed, transcriptional changes in genes associated with the general stress responses, including the oxidative stress response were among the major differences observed. Accordingly, the K3 strain was less resistant to reactive oxygen species (ROS) than the wild-type strain. In addition, the pst mutant demonstrated reduced expression of genes involved in lipopolysaccharide modifications and coding for cell surface components such as type 1 and F9 fimbriae. Phenotypic tests also established that the pst mutant was impaired in its capacity to produce type 1 fimbriae, as demonstrated by western blotting and agglutination of yeast cells, when compared to wild-type APEC strain χ7122.

Conclusion

Overall, our data elucidated the effects of a pst mutation on the transcriptional response, and further support the role of the Pho regulon as part of a complex network contributing to phosphate homeostasis, adaptive stress responses, and E. coli virulence.