Sulfate-reducing bacteria and sulfur-oxidizing bacteria interactions at redox interfaces: Implications for mercury methylation.

Methylmercury (MeHg), the most neurotoxic and bioaccumulative mercury (Hg) species, poses significant risks to human and ecosystem health. Predicting these risks requires elucidating the drivers of MeHg production, which peaks at redox interfaces in aquatic systems where the primary Hg methylators, sulfate-reducing bacteria (SRB), are most active. Elevated Hg(II) methylation at these zones is primarily driven by the active sulfur cycling, primarily mediated by Hg-methylating SRB and sulfur-oxidizing bacteria (SOB) interactions. This review explores possible mechanisms enhancing Hg(II) methylation at redox interfaces, focusing on: 1) coupling between Hg(II) methylation and inorganic sulfur cycling; 2) syntrophic coexistence of SRB and SOB; and 3) SRB-SOB interactions that enhance Hg(II) bioavailability and microbial activity. We propose that SOB mitigate HgS precipitation by rapidly oxidizing SRB-derived sulfide, thereby increasing Hg(II) bioavailability. Concurrently, SOB generate sulfate (SO42-), sustaining Hg-methylating SRB metabolic activity and promoting MeHg production. While previous studies highlight these synergies, direct evidence linking SOB activity to Hg speciation remains scarce. Future research is needed to understand whether SOB directly internalize or excrete Hg(II) and MeHg, and how extracellular metabolites (e.g., exopolysaccharides, thiols) alter Hg speciation and bioavailability. Additionally, although microbial interactions enhance SRB and SOB growth in coculture, the pathways mediating these interactions are poorly characterized. Resolving these knowledge gaps is helpful in mitigating MeHg risks in redox-stratified environments.