Altering the anaerobic transcription factor FNR confers a hemolytic phenotype on Escherichia coli K12

Proc Natl Acad Sci U S A. 1998 Sep 1;95(18):10449-52. doi: 10.1073/pnas.95.18.10449.

Abstract

The recent outbreaks of Escherichia coli O157-associated food poisoning have focused attention on the virulence determinants of E. coli. Here, it is reported that single base substitutions in the fnr gene encoding the oxygen-responsive transcription regulator FNR (fumarate and nitrate reduction regulator) are sufficient to confer a hemolytic phenotype on E. coli K12, the widely used laboratory strain. The mechanism involves enhancing the expression of a normally dormant hemolysin gene (hlyE) located in the E. coli chromosome. The mutations direct single amino acid substitutions in the activating regions (AR1 and AR3) of FNR that contact RNA polymerase. It is concluded that altering a resident transcription regulator, or acquisition of a competent heterologous regulator, could generate a pool of hemolytic, and therefore more virulent, strains of E. coli in nature.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Amino Acid Substitution
  • Bacterial Proteins / chemistry
  • Bacterial Proteins / genetics
  • Bacterial Proteins / metabolism*
  • Base Sequence
  • CDC2-CDC28 Kinases*
  • Cyclin A / metabolism
  • Cyclin-Dependent Kinase 2
  • Cyclin-Dependent Kinases / metabolism
  • DNA Primers
  • Escherichia coli / genetics*
  • Escherichia coli Proteins*
  • Hemolysis / genetics*
  • Iron-Sulfur Proteins / chemistry
  • Iron-Sulfur Proteins / genetics
  • Iron-Sulfur Proteins / metabolism*
  • Molecular Sequence Data
  • Phenotype
  • Protein Binding
  • Protein Serine-Threonine Kinases / metabolism
  • Transcription Factors / chemistry
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*

Substances

  • Bacterial Proteins
  • Cyclin A
  • DNA Primers
  • Escherichia coli Proteins
  • FNR protein, E coli
  • Iron-Sulfur Proteins
  • Transcription Factors
  • Protein Serine-Threonine Kinases
  • CDC2-CDC28 Kinases
  • Cyclin-Dependent Kinase 2
  • Cyclin-Dependent Kinases