The Effect of Cell Growth Phase on the Regulatory Cross-Talk between Flagellar and Spi1 Virulence Gene Expression
Flagellar-mediated motility is fundamental to Salmonella pathogenesis, which takes the lives of hundreds of thousands of people each year. The genes of the Salmonella pathogenicity island 1 and those of the flagellar regulon are part of the same transcriptional hierarchy. We report the novel finding where the key control of this network takes place at the flhDC promoter region. We followed the transcription from the two “live” flhDC promoters as a function of the cell growth phase. P1 comes on early in the cell cycle, while P5 comes on late. Transcription of P5 is HilD dependent, which represents a totally new finding and Salmonella specific: there is no HilD in E. coli flhDC control, no P5 transcription. P1 & P5 can express flhDC to equivalent levels, yet only P1- dependent expression produces motility UNLESS we artificially induce P5 EARLY in the cell cycle. This work is the foundation for the cell cycle stages a Salmonella bacterium experiences during host infection. This is a significant conceptual advance in Salmonella pathogenesis: one can no longer consider gene regulation at 37°C and OD 0.6 as a reflection of the Salmonella infection cycle; the whole cell growth cycle must be considered in understanding this complex biological processes.
Vyšlo v časopise:
The Effect of Cell Growth Phase on the Regulatory Cross-Talk between Flagellar and Spi1 Virulence Gene Expression. PLoS Pathog 10(3): e32767. doi:10.1371/journal.ppat.1003987
Kategorie:
Research Article
prolekare.web.journal.doi_sk:
https://doi.org/10.1371/journal.ppat.1003987
Souhrn
Flagellar-mediated motility is fundamental to Salmonella pathogenesis, which takes the lives of hundreds of thousands of people each year. The genes of the Salmonella pathogenicity island 1 and those of the flagellar regulon are part of the same transcriptional hierarchy. We report the novel finding where the key control of this network takes place at the flhDC promoter region. We followed the transcription from the two “live” flhDC promoters as a function of the cell growth phase. P1 comes on early in the cell cycle, while P5 comes on late. Transcription of P5 is HilD dependent, which represents a totally new finding and Salmonella specific: there is no HilD in E. coli flhDC control, no P5 transcription. P1 & P5 can express flhDC to equivalent levels, yet only P1- dependent expression produces motility UNLESS we artificially induce P5 EARLY in the cell cycle. This work is the foundation for the cell cycle stages a Salmonella bacterium experiences during host infection. This is a significant conceptual advance in Salmonella pathogenesis: one can no longer consider gene regulation at 37°C and OD 0.6 as a reflection of the Salmonella infection cycle; the whole cell growth cycle must be considered in understanding this complex biological processes.
Zdroje
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