Abundance and expression of hgcAB genes and mercury availability jointly explain methylmercury formation in stratified brackish waters

Abstract

Neurotoxic methylmercury (MeHg) is formed by microbial methylation of inorganic divalent Hg (HgII) and constitutes severe environmental and human health risks. The methylation is enabled by hgcA and hgcB genes, but it is not known if the associated molecular-level processes are rate-limiting or enable accurate prediction of MeHg formation in nature. In this study, we investigated the relationships between hgcA genes and MeHg across redox stratified water columns in the brackish Baltic Sea. We found that the abundance of hgcA genes and transcripts combined with the concentration of dissolved HgII-sulfide species were strong predictors of both HgII methylation rate and MeHg concentration, implying their roles as principal joint drivers of MeHg formation in these systems. In establishing relationships between hgcA genes and MeHg, we advance the fundamental understanding of mechanistic principles governing MeHg formation in nature and enable refined predictions of MeHg levels in coastal seas in response to the accelerating spread of oxygen deficient zones.