Bacillus subtilis Response to Mercury Toxicity: A Defense Mediated by Sulphur-Rich Molecules and Oxidative Prevention Systems

TL;DR

This study explores how the bacterium Bacillus subtilis defends against mercury toxicity using sulfur-rich molecules and oxidative prevention systems.

Contribution

The study reveals novel defense mechanisms in B. subtilis against mercury-induced oxidative stress and DNA damage.

Findings

Hg(II) exposure increases mutation frequency in B. subtilis, indicating genotoxic effects.

RNA-seq shows upregulation of genes for metal efflux and sulfur molecule synthesis.

Downregulation of iron metabolism genes suggests a link to ROS imbalance.

Abstract

Upon reacting with cellular components, Hg(II) ions elicit the production of reactive oxygen species (ROS). While the ROS-promoted cytotoxic and genotoxic effects induced by Hg(II) have been widely described in eukaryotes, such effects have been less studied in bacteria. In this work, the prokaryotic environmental model Bacillus subtilis was employed to evaluate the cytotoxic and genotoxic impact of Hg(II) over strains proficient or deficient in SOS, general stress and antioxidant responses, as well as the global transcriptional response elicited by this ion. The exposure to HgCl2 significantly increased the mutation frequency to rifampicin resistance (RifR) in WT and mutant strains, suggesting a major contribution of these pathways in counteracting the genotoxic effects of Hg(II). Detection of A → T and C → G transversion mutations in the rpoB gene of Hg(II)-exposed cells suggested the generation of 8-oxo-guanines (8-OxoGs) and other oxidized DNA bases. The RNA-seq study revealed upregulation of genes involved in efflux and/or reduction of metal ions, synthesis of sulfur-containing molecules, and downregulation of genes implicated in iron metabolism and cell envelope stress. Therefore, our results indicate that metal extrusion and scavenging of Hg(II) by thiol-rich molecules may constitute a line of defense of B. subtilis that counteracts the noxious effects of ROS resulting from an imbalance in iron metabolism elicited by this ion.

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