Multiple co-regulatory elements and IHF are necessary for the control of fimB expression in response to sialic acid and N-acetylglucosamine in Escherichia coli K-12

Mol Microbiol. 2007 Feb;63(4):1223-36. doi: 10.1111/j.1365-2958.2006.05583.x.


Expression of the FimB recombinase, and hence the OFF-to-ON switching of type 1 fimbriation in Escherichia coli, is inhibited by sialic acid (Neu(5)Ac) and by GlcNAc. NanR (Neu(5)Ac-responsive) and NagC (GlcNAc-6P-responsive) activate fimB expression by binding to operators (O(NR) and O(NC1) respectively) located more than 600 bp upstream of the fimB promoter within the large (1.4 kb) nanC-fimB intergenic region. Here it is demonstrated that NagC binding to a second site (O(NC2)), located 212 bp closer to fimB, also controls fimB expression, and that integration host factor (IHF), which binds midway between O(NC1) and O(NC2), facilitates NagC binding to its two operator sites. In contrast, IHF does not enhance the ability of NanR to activate fimB expression in the wild-type background. Neither sequences up to 820 bp upstream of O(NR), nor those 270 bp downstream of O(NC2), are required for activation by NanR and NagC. However, placing the NanR, IHF and NagC binding sites closer to the fimB promoter enhances the ability of the regulators to activate fimB expression. These results support a refined model for how two potentially key indicators of host inflammation, Neu(5)Ac and GlcNAc, regulate type 1 fimbriation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylglucosamine / pharmacology*
  • Binding Sites
  • DNA-Binding Proteins / drug effects
  • DNA-Binding Proteins / genetics*
  • DNA-Binding Proteins / metabolism
  • Escherichia coli K12 / drug effects
  • Escherichia coli K12 / genetics*
  • Escherichia coli K12 / physiology
  • Escherichia coli Proteins / drug effects
  • Escherichia coli Proteins / genetics*
  • Escherichia coli Proteins / metabolism
  • Gene Expression Regulation, Bacterial
  • Integrases / drug effects
  • Integrases / genetics*
  • Integrases / metabolism
  • Integration Host Factors / drug effects
  • Integration Host Factors / genetics
  • Integration Host Factors / metabolism*
  • Methylation
  • Mutagenesis
  • N-Acetylneuraminic Acid / pharmacology*
  • Promoter Regions, Genetic
  • Regulatory Sequences, Nucleic Acid
  • Repressor Proteins / genetics
  • Repressor Proteins / metabolism
  • Transcription Factors / genetics
  • Transcription Factors / metabolism


  • DNA-Binding Proteins
  • Escherichia coli Proteins
  • Integration Host Factors
  • NanR protein, E coli
  • Repressor Proteins
  • Transcription Factors
  • fimB protein, E coli
  • nagC protein, E coli
  • Integrases
  • N-Acetylneuraminic Acid
  • Acetylglucosamine