The virulence regulator Rns activates the expression of CS14 Pili

Maria Del Rocio Bodero, George Munson

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Although many viral and bacterial pathogens cause diarrhea, enterotoxigenic E. coli (ETEC) is one of the most frequently encountered in impoverished regions where it is estimated to kill between 300,000 and 700,000 children and infants annually. Critical ETEC virulence factors include pili which mediate the attachment of the pathogen to receptors in the intestinal lumen. In this study we show that the ETEC virulence regulator Rns positively regulates the expression of CS14 pili. Three Rns binding sites were identified upstream of the CS14 pilus promoter centered at −34.5, −80.5, and −155.5 relative to the Rns-dependent transcription start site. Mutagenesis of the promoter proximal site significantly decreased expression from the CS14 promoter. In contrast, the contribution of Rns bound at the promoter distal site was negligible and largely masked by occupancy of the promoter proximal site. Unexpectedly, Rns bound at the site centered at −80.5 had a slight but statistically significant inhibitory effect upon the pilin promoter. Nevertheless, this weak inhibitory effect was not sufficient to overcome the substantial promoter activation from Rns bound to the promoter proximal site. Thus, CS14 pili belong to a group of pili that depend upon Rns for their expression.

Original languageEnglish (US)
Article number120
JournalGenes
Volume7
Issue number12
DOIs
StatePublished - Dec 8 2016

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Enterotoxigenic Escherichia coli
Virulence
Fimbriae Proteins
Transcription Initiation Site
Virulence Factors
Mutagenesis
Diarrhea
Binding Sites

Keywords

  • Activator
  • Enterotoxigenic E. Coli
  • ETEC
  • Pili
  • Rns

ASJC Scopus subject areas

  • Genetics
  • Genetics(clinical)

Cite this

The virulence regulator Rns activates the expression of CS14 Pili. / Bodero, Maria Del Rocio; Munson, George.

In: Genes, Vol. 7, No. 12, 120, 08.12.2016.

Research output: Contribution to journalArticle

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