Transcriptional Control of by an ArsR-Like Regulator in ND132.

The gene pair encodes mercury (Hg) methylation capability in a diverse group of microorganisms, but its evolution and transcriptional regulation remain unknown. Working from the possibility that the evolutionary function of HgcAB may not be Hg methylation, we test a possible link to arsenic resistance. Using model Hg methylator Pseudodesulfovibrio mercurii ND132, we evaluated transcriptional control of by a putative ArsR encoded upstream and cotranscribed with . This regulator shares homology with ArsR repressors of arsenic resistance and -adenosylhomocysteine (SAH)-responsive regulators of methionine biosynthesis but is distinct from other ArsR/SahR proteins in . Using quantitative PCR (qPCR) and RNA sequencing (RNA-seq) transcriptome analyses, we confirmed this ArsR regulates transcription and is responsive to arsenic and SAH. Additionally, RNA-seq indicated a possible link between activity and arsenic transformations, with significant upregulation of other ArsR-regulated arsenic resistance operons alongside . Interestingly, wild-type ND132 was less sensitive to As(V) (but not As(III)) than an knockout strain, supporting the idea that may be linked to arsenic resistance. Arsenic significantly impacted rates of Hg methylation by ND132; however, responses varied with culture conditions. Differences in growth and metabolic activity did not account for arsenic impacts on methylation. While arsenic significantly increased expression, gene and transcript abundance was not a good predictor of Hg methylation rates. Taken together, these results support the idea that Hg and As cycling are linked in ND132. Our results may hold clues to the evolution of and the controls on Hg methylation in nature. This work reveals a link between microbial mercury methylation and arsenic resistance and may hold clues to the evolution of mercury methylation genes (). Microbes with produce methylmercury, a strong neurotoxin that readily accumulates in the food web. This study addresses a critical gap in our understanding about the environmental factors that control expression. We show that expression is controlled by an ArsR-like regulator responsive to both arsenic and -adenosylhomocysteine in our model organism, ND132. Exposure to arsenic also significantly impacted ND132 mercury methylation rates. However, expression of was not always a good predictor of Hg methylation rates, highlighting the roles of Hg bioavailability and other biochemical mechanisms in methylmercury production. This study improves our understanding of the controls on expression, which is needed to better predict environmental methylmercury production.