Cobalt targets multiple metabolic processes in Salmonella enterica

J Bacteriol. 2007 Nov;189(21):7774-81. doi: 10.1128/JB.00962-07. Epub 2007 Aug 24.


Cobalt is essential for growth of Salmonella enterica and other organisms, yet this metal can be toxic when present in excess. Wild-type Salmonella exhibits several metabolic defects when grown in the presence of cobalt, some of which generate visible growth consequences. Work herein identifies sulfur assimilation, iron homeostasis, and Fe-S cluster metabolism as targets for cobalt toxicity. In each case it is proposed that cobalt exerts its effect by one of two mechanisms: direct competition with iron or indirectly through a mechanism that involves the status of reduced thiols in the cell. Cobalt toxicity results in decreased siroheme production, increased expression of the Fur regulon, and decreased activity of Fe-S cluster proteins. The consequences of reduced sulfite reductase activity in particular are exacerbated by the need for glutathione in cobalt resistance. Significantly, independent metabolic perturbations could be detected at cobalt concentrations below those required to generate a detectable growth defect.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Bacterial Proteins / metabolism
  • Chlorides
  • Cobalt / pharmacology*
  • Ferric Compounds / pharmacology
  • Genotype
  • Kinetics
  • Nitrite Reductases / metabolism
  • Salmonella enterica / drug effects
  • Salmonella enterica / genetics
  • Salmonella enterica / growth & development
  • Salmonella enterica / metabolism*
  • Sulfides / metabolism


  • Bacterial Proteins
  • Chlorides
  • Ferric Compounds
  • Sulfides
  • Cobalt
  • Nitrite Reductases
  • ferric chloride