Inducible plasmid-determined resistance to arsenate, arsenite, and antimony(III) in Escherichia coli and Staphylococcus aureus

Plasmids in both E. coli and S. aureus contain an 'operon' that confers resistances to arsenate, arsenite, and antimony(III) salts. The systems were always inducible. All 3 salts, arsenate, arsenite, and antimony(III), were inducers. Mutants and a cloned deoxyribonucleic acid fragment from plasmid pI258 in S. aureus have lost arsenate resistance but retained resistances to arsenite and antimony, demonstrating that separate genes are involved. Arsenate-resistant arsenite-sensitive S. aureus plasmid mutants were also isolated. In E. coli, plasmid-determined arsenate resistance and reduced uptake were additive to that found with chromosomal arsenate resistance mutants. Arsenate resistance was due to reduced uptake of arsenate by the induced plasmid-containing cells. Under conditions of high arsenate, when some uptake could be demonstrated with the induced resistant cells, the arsenate was rapidly lost by the cells in the absence of extracellular phosphate. Sensitive cells retained arsenate under these conditions. When phosphate was added, phosphate-arsenate exchange occurred. High phosphate in the growth medium protected cells from arsenate, but not from arsenite or antimony(III) toxicity. The mechanisms of arsenite or antimony resistance are unknown. However, arsenite was not oxidized to less toxic arsenate. Since cell-free medium 'conditioned' by prior growth of induced resistant cells with toxic levels of arsenite or antimony(III) retained the ability to inhibit the growth of sensitive cells, the mechanism of arsenite and antimony resistance does not involve conversion of AsO ₂ ^- or SbO ⁺ to less toxic forms or binding by soluble thiols excreted by resistant cells.