Adaptation to metal(loid)s in strain Mucilaginibacter rubeus P2 involves novel arsenic resistance genes and mechanisms

Abstract

Arsenic is a ubiquitous environmental toxi substance that affects human health. Compared to inorganic arsenicals, reduced organoarsenicals are more toxic, and some of them are recognized as antibiotics, such as methylarsenite [MAs(III)] and arsinothricin (2-amino-4-(hydroxymethylarsinoyl)butanoate, or AST). To date, organoarsenicals such as MAs(V) and roxarsone [Rox(V)] are still used in agriculture and animal husbandry. How bacteria deal with both inorganic and organoarsenic species is unclear. Recently, we identified an environmental isolate Mucilaginibacter rubeus P2 that has adapted to high arsenic and antinomy levels by triplicating an arsR-mrarsUBact-arsN-arsC-(arsRhp)-hp-acr3-mrme1Bact-mrme2Bactgene cluster. Heterologous expression of mrarsMBact, mrarsUBact, mrme1Bact and mrme2Bact, encoding putative arsenic resistance determinants, in the arsenic hypersensitive strain Escherichia coli AW3110 conferred resistance to As(III), As(V), MAs(III) or Rox(III). Our data suggest that metalloid exposure promotes plasticity in arsenic resistance systems, enhancing host organism adaptation to metalloid stress.