Comprehensive genomic and proteomic profiling reveal Acinetobacter johnsonii JH7 responses to Sb(III) toxicity.

Antimony (Sb) pollution poses a severe health threat to ecosystems. However, the toxic effects of Sb on biota are far from being elucidated. One of the unresolved questions is the molecular signal pathways underlying microbial adaptation to excess antimonite or Sb(III) exposure. The response of a Sb(III)-resistant bacterium Acinetobacter. johnsonii JH7 to Sb(III) stress was investigated using genomic and proteomic profiling. Sb(III) induced the formation of reactive oxygen species thereby leading to oxidative stress and the up-regulation of antioxidant enzyme activities. In addition, two important operons (ars and pst) playing critical roles in this cellular response were identified. The ars proteins functioned cooperatively to expel Sb(III) thereby decreasing antimonite toxicity. Downregulation of the phosphate-specific transporter might reduce the uptake of Sb(V) while hindering phosphorus assimilation. Interaction of Sb(III) with JH7 strain cells also affected peptide syntheses and folding, energy conversion, and stability of the cellular envelope. The present study provides for the first time a global map of cellular adaptation to excess Sb(III). Such information is potentially useful to future Sb pollution remediation strategies.