Beclomethasone aerosol in childhood asthma.

Abstract

The <i>hgcAB</i> 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 <i>Pseudodesulfovibrio mercurii</i> ND132, we specifically evaluated transcriptional control of <i>hgcAB</i> by a putative ArsR encoded upstream and co-transcribed with <i>hgcAB</i>. This regulator shares homology with ArsR repressors of arsenic resistance and S-adenosyl-homocysteine (SAH) responsive regulators of methionine biosynthesis but is distinct from other ArsR/SahR in <i>Pseudodesulfovibrio mercurii</i> ND132. Using qPCR and RNA-seq analyses we confirmed this ArsR regulates <i>hgcAB</i> transcription, and is responsive to arsenic and SAH. Additionally, RNA-seq indicated a possible link between <i>hgcAB</i> activity and arsenic transformations by <i>Pseudodesulfovibrio mercurii</i> ND132, with significant up-regulation of other ArsR-regulated arsenic resistance operons alongside <i>hgcAB</i>. Interestingly, wild-type ND132 was less sensitive to AsV (but not AsIII) than an <i>hgcAB</i> knockout strain, supporting the idea that <i>hgcAB</i> may be linked to arsenic resistance. Arsenic significantly impacted Hg-methylation rates by ND132, however, responses varied with culture conditions. Differences in growth and overall metabolic activity did not account for arsenic impacts on methylation. One goal of this research is to better predict MeHg production in nature. However, we found that <i>hgcAB</i> gene and transcript abundance was not a good predictor of Hg-methylation rates. Our finding that <i>hgcAB</i> activity is linked to arsenic may hold clues to the possible environmental drivers of horizontal transfer of <i>hgcAB</i>.