Expanded Diversity and Phylogeny of mer Genes Broadens Mercury Resistance Paradigms and Reveals an Origin for MerA Among Thermophilic Archaea Original paper

What was studied?

This original research study used large-scale bioinformatics to map where mercury detoxification genes occur across prokaryotes and to infer how those genes evolved. The authors screened 84,032 bacterial and archaeal genomes, including isolate genomes, metagenome-assembled genomes, and single-cell genomes, for mercuric reductase (MerA), which reduces Hg(II) to volatile Hg(0), and organomercury lyase (MerB), which breaks the carbon–mercury bond in organomercury compounds such as methylmercury and generates Hg(II) that usually requires MerA for completion of detoxification.

Who was studied?

The “subjects” were publicly available microbial genomes spanning broad environmental and host-associated contexts rather than human participants. The dataset included thousands of bacterial and archaeal lineages across many phyla, plus plasmid genomes, which allowed the authors to identify both core taxonomic patterns and evidence of horizontal gene transfer. Notably, the paper includes examples of mer genes in organisms relevant to host-associated microbiomes, such as a Bacillus cereus strain isolated from a mouse gut sample, alongside many taxa common in soils, sediments, hot springs, aquifers, and other mercury-impacted habitats.

What were the most important findings?

MerA appeared in 7.8% of analyzed genomes and MerB in 2.1%, greatly expanding the known taxonomic range of mercury resistance compared with earlier inventories and identifying MerA and MerB in multiple archaeal and bacterial phyla not previously recognized to encode them. A key microbiome-relevant signal was the major microbial association between mer genes and diverse bacterial genera that include gut- and pathogen-adjacent groups; for example, many MerB-only genomes clustered within genera such as Clostridioides, Clostridium, Staphylococcus, Corynebacterium, Streptomyces, Enterobacter, and Mycobacterium/Mycobacteroides, implying that organomercury cleavage capacity may be more common than expected in clinically relevant lineages. Strikingly, just over half of MerB-containing genomes lacked MerA, which challenges the classic “MerB feeds MerA” detox model and supports alternative intracellular strategies for handling the Hg(II) produced by MerB, including sulfur-based buffering or sequestration, redox-homeostasis–linked Hg(II) reduction, and iron-coupled processes. Phylogeny placed the origin of MerA in thermophilic Archaea (Thermoprotei) consistent with geothermal mercury exposure, while MerB appeared to be recruited later, more consistent with mesophilic settings where methylmercury production is more likely.

What are the greatest implications of this study?

Clinically, this work reframes mercury-handling capacity as a distributed microbial trait that can plausibly exist in host-associated communities, not only in obvious environmental specialists, which matters when considering dietary methylmercury exposure and the potential for microbial demethylation or mercury transformations in the gut. Mechanistically, the frequent MerB-without-MerA pattern signals that mercury risk assessments and microbiome signature databases should not treat mer operons as a single fixed unit; instead, they should track MerA and MerB separately and consider co-occurring non-mer redox and sulfur-handling pathways that could complete detoxification or shift mercury speciation. Environmentally, the expanded diversity and lateral transfer of mer genes suggest strong selection pressure and a high likelihood of gene movement across ecosystems, which can influence how methylmercury is produced, degraded, and ultimately enters food webs.