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Papers In Press, published online ahead of print February 25, 2004
Pathogen Genomics, National Research Council of Canada, Ottawa, Ontario K1A 0R6
Corresponding Author: Christine.Szymanski{at}nrc-cnrc.gc.ca
We examined two variants of the genome-sequenced strain, Campylobacter jejuni NCTC11168, which show marked differences in their virulence properties including colonization of poultry, invasion of Caco-2 cells, and motility. Transcript profiles obtained from whole genome DNA microarrays and proteome analyses demonstrated that these differences are reflected in late flagellar structural components and in virulence factors including those involved in flagellar glycosylation, and cytolethal distending toxin production. We identified putative s28 and s54 promoters for many of the affected genes, and found that greater differences in expression were observed for s28-controlled genes. Inactivation of the gene encoding s28, fliA, resulted in an unexpected increase in transcripts with s54 promoters, as well as decreased transcription of s28-regulated genes. This was unlike the transcription profile observed for the attenuated C. jejuni variant, suggesting that the reduced virulence of this organism was not entirely due to impaired function of s28. However, inactivation of flhA, an important component of the flagellar export apparatus, resulted in expression patterns similar to that of the attenuated variant. These findings indicate that the flagellar regulatory system plays an important role in campylobacter pathogenesis and that flhA is a key element involved in the coordinate regulation of late flagellar genes and of virulence factors in C. jejuni. Furthermore, we provide a model for flagellar regulation, which forms a foundation for the study of the unique regulatory networks in this important human pathogen.
J. Biol. Chem, 10.1074/jbc.M401134200
Submitted on February 2, 2004
Revised on February 25, 2004
Accepted on February 24, 2004
Genome-wide expression analyses of campylobacter jejuni NCTC11168 reveals coordinate regulation of motility and virulence by flhA
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