Genome-wide transcriptional response of an avian pathogenic Escherichia coli (APEC) pst mutant.
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 chi7122 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 chi7122.


CONCLUSIONS
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.
Crépin
Sébastien
S
Groupe de Recherche sur les Maladies Infectieuses du Porc (GREMIP), Université de Montréal, Faculté de Médecine Vétérinaire, Saint-Hyacinthe, Québec, Canada. sebastien.crepin@iaf.inrs.ca
Lamarche
Martin G
MG
Garneau
Philippe
P
Séguin
Julie
J
Proulx
Julie
J
Dozois
Charles M
CM
Harel
Josée
J
D000818:Animals; D001717:Birds / Q000382:microbiology; D004926:Escherichia coli / Q000235:genetics* / Q000378:metabolism; D029968:Escherichia coli Proteins / Q000235:genetics / Q000378:metabolism; D010861:Fimbriae, Bacterial / Q000235:genetics / Q000378:metabolism; D020869:Gene Expression Profiling; D015964:Gene Expression Regulation, Bacterial; D016680:Genome, Bacterial; D009154:Mutation; D020411:Oligonucleotide Array Sequence Analysis; D009876:Operon; D018384:Oxidative Stress; D012329:RNA, Bacterial / Q000235:genetics; D017382:Reactive Oxygen Species / Q000378:metabolism; D018085:Regulon; D014158:Transcription, Genetic
D029968:Escherichia coli Proteins; D012329:RNA, Bacterial; D017382:Reactive Oxygen Species