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Discovering CsgD Regulatory Targets in Salmonella Biofilm Using Chromatin Immunoprecipitation and High-Throughput Sequencing (ChIP-seq)
Published on: January 18, 2020
Cobalt targets multiple metabolic processes in Salmonella enterica
Michael P Thorgersen1, Diana M Downs
1Department of Bacteriology, University of Wisconsin-Madison, 1550 Linden Dr., Madison, WI 53706, USA.
Journal of Bacteriology
|August 28, 2007
Summary
Cobalt is essential but toxic to Salmonella. Excess cobalt disrupts sulfur assimilation, iron homeostasis, and Fe-S cluster metabolism, impacting cell growth and function.
Area of Science:
- Microbiology
- Biochemistry
- Toxicology
Background:
- Cobalt is a vital nutrient for Salmonella enterica and other organisms.
- However, excessive cobalt concentrations can lead to toxicity and metabolic dysfunction.
Purpose of the Study:
- To identify the specific metabolic targets of cobalt toxicity in Salmonella.
- To elucidate the mechanisms by which cobalt exerts its toxic effects.
Main Methods:
- Investigated metabolic defects in wild-type Salmonella grown with cobalt.
- Analyzed the impact of cobalt on sulfur assimilation, iron homeostasis, and Fe-S cluster metabolism.
Main Results:
- Cobalt toxicity affects sulfur assimilation, iron homeostasis, and Fe-S cluster metabolism.
- Cobalt interferes with iron-dependent processes and cellular thiol status.
- Observed decreased siroheme production, increased Fur regulon expression, and reduced Fe-S cluster protein activity.
Conclusions:
- Cobalt toxicity in Salmonella is mediated by direct iron competition or indirect effects on cellular thiols.
- Reduced sulfite reductase activity is a key consequence, exacerbated by glutathione requirements for cobalt resistance.
- Metabolic disruptions occur at cobalt concentrations below those causing visible growth defects.
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