Molecular mechanism for establishment of signal-dependent regulation in the PhoP/PhoQ system

Wei Kong, Natasha Weatherspoon, Yixin Shi

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

In this report, we demonstrate that H-NS is essential for establishing the Mg2+-responsive transcriptional regulation of the PhoP regulon in Salmonella. Deletion of this regulatory gene abolished the transcriptional repression of PhoP-activated genes when bacteria were grown in high environmental Mg2+, thus stimulating expression of phoP and other PhoP regulon genes. In the absence of H-NS, transcriptional activation was PhoP-dependent for those genes only activated by PhoP, but was PhoP-independent for those genes activated by both PhoP and SlyA. The H-NS protein footprints the phoP promoter in a sequence located upstream of the PhoP box; mutation of this cis-acting factor abolished transcriptional repression of the phoP gene equivalent to the phenotype exhibited in the hns mutant. Further results showed that H-NS gel shifts other PhoP regulon promoters, indicating that a PhoP-activated gene would be transcriptionally repressed via direct H-NS binding and inhibition of its activator PhoP. Furthermore, H-NS footprints a newly identified SlyA box and the reverse PhoP box in the pagC promoter, suggesting that both SlyA and PhoP compete with this regulatory protein. Therefore, H-NS should pair with SlyA and PhoP to establish a forward regulatory loop to regulate expression of pagC, and perhaps other PhoP- and SlyA-dependent genes.

Original languageEnglish (US)
Pages (from-to)16612-16621
Number of pages10
JournalJournal of Biological Chemistry
Volume283
Issue number24
DOIs
StatePublished - Jun 13 2008

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Genes
Regulon
Protein Footprinting
Salmonella
Regulator Genes
Transcriptional Activation
Gels
Bacteria
Proteins
Phenotype
Chemical activation
Mutation

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology

Cite this

Molecular mechanism for establishment of signal-dependent regulation in the PhoP/PhoQ system. / Kong, Wei; Weatherspoon, Natasha; Shi, Yixin.

In: Journal of Biological Chemistry, Vol. 283, No. 24, 13.06.2008, p. 16612-16621.

Research output: Contribution to journalArticle

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N2 - In this report, we demonstrate that H-NS is essential for establishing the Mg2+-responsive transcriptional regulation of the PhoP regulon in Salmonella. Deletion of this regulatory gene abolished the transcriptional repression of PhoP-activated genes when bacteria were grown in high environmental Mg2+, thus stimulating expression of phoP and other PhoP regulon genes. In the absence of H-NS, transcriptional activation was PhoP-dependent for those genes only activated by PhoP, but was PhoP-independent for those genes activated by both PhoP and SlyA. The H-NS protein footprints the phoP promoter in a sequence located upstream of the PhoP box; mutation of this cis-acting factor abolished transcriptional repression of the phoP gene equivalent to the phenotype exhibited in the hns mutant. Further results showed that H-NS gel shifts other PhoP regulon promoters, indicating that a PhoP-activated gene would be transcriptionally repressed via direct H-NS binding and inhibition of its activator PhoP. Furthermore, H-NS footprints a newly identified SlyA box and the reverse PhoP box in the pagC promoter, suggesting that both SlyA and PhoP compete with this regulatory protein. Therefore, H-NS should pair with SlyA and PhoP to establish a forward regulatory loop to regulate expression of pagC, and perhaps other PhoP- and SlyA-dependent genes.

AB - In this report, we demonstrate that H-NS is essential for establishing the Mg2+-responsive transcriptional regulation of the PhoP regulon in Salmonella. Deletion of this regulatory gene abolished the transcriptional repression of PhoP-activated genes when bacteria were grown in high environmental Mg2+, thus stimulating expression of phoP and other PhoP regulon genes. In the absence of H-NS, transcriptional activation was PhoP-dependent for those genes only activated by PhoP, but was PhoP-independent for those genes activated by both PhoP and SlyA. The H-NS protein footprints the phoP promoter in a sequence located upstream of the PhoP box; mutation of this cis-acting factor abolished transcriptional repression of the phoP gene equivalent to the phenotype exhibited in the hns mutant. Further results showed that H-NS gel shifts other PhoP regulon promoters, indicating that a PhoP-activated gene would be transcriptionally repressed via direct H-NS binding and inhibition of its activator PhoP. Furthermore, H-NS footprints a newly identified SlyA box and the reverse PhoP box in the pagC promoter, suggesting that both SlyA and PhoP compete with this regulatory protein. Therefore, H-NS should pair with SlyA and PhoP to establish a forward regulatory loop to regulate expression of pagC, and perhaps other PhoP- and SlyA-dependent genes.

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