Abstract

Bacterial siderophores may enhance pathogenicity by scavenging iron, but their expression has been proposed to exert a substantial metabolic cost. Here we describe a combined metabolomic-genetic approach to determine how mutations affecting the virulence-associated siderophore yersiniabactin affect the Escherichia coli primary metabolome. Contrary to expectations, we did not find yersiniabactin biosynthesis to correspond to consistent metabolomic shifts. Instead, we found that targeted deletion of ybtU or ybtA, dissimilar genes with similar roles in regulating yersiniabactin expression, were associated with a specific shift in arginine pathway metabolites during growth in minimal media. This interaction was associated with high arginine levels in the model uropathogen Escherichia coli UTI89 compared to its ybtU and ybtA mutants and the K12 strain MG1655, which lacks yersiniabactin-associated genes. Because arginine is not a direct yersiniabactin biosynthetic substrate, these findings show that virulence-associated secondary metabolite systems may shape bacterial primary metabolism independently of substrate consumption.

Original languageEnglish
Pages (from-to)5547-5554
Number of pages8
JournalJournal of Proteome Research
Volume10
Issue number12
DOIs
StatePublished - Dec 2 2011

Keywords

  • Escherichia coli
  • arginine biosynthesis
  • metabolomics
  • primary metabolism
  • siderophore
  • ybtA
  • ybtU
  • yersiniabactin

Fingerprint

Dive into the research topics of 'Yersinia high pathogenicity Island genes modify the Escherichia coli primary metabolome independently of siderophore production'. Together they form a unique fingerprint.

Cite this