Efflux-mediated antiseptic resistance gene qacA from Staphylococcus aureus: common ancestry with tetracycline- and sugar-transport proteins

Authors

  • D. A. Rouch,

    1. Department of Microbiology, Monash University, Clayton, Victoria 3168, Australia.
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    • School of Biological Sciences, Birmingham University, PO Box 363, Birmingham B15 2TT, UK

  • D. S. Cram,

    1. Department of Microbiology, Monash University, Clayton, Victoria 3168, Australia.
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    • Walter and Eliza Hall Institute for Medical Research, Parkville, Victoria 3052, Australia.

  • D. Di Berardino,

    1. Department of Microbiology, Monash University, Clayton, Victoria 3168, Australia.
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  • T. G. Littlejohn,

    1. Department of Microbiology, Monash University, Clayton, Victoria 3168, Australia.
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  • R. A. Skurray

    Corresponding author
    1. Department of Microbiology, Monash University, Clayton, Victoria 3168, Australia.
    • *For correspondence. Tel. (3) 565 4827; Fax (3) 565 4811.

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Summary

Resistance to intercalating dyes (ethidium, acriflavine) and other organic cations, such as quaternary ammonium-type antiseptic compounds, mediated by the Staphylococcus aureus ptasmid pSK1 is specified by an energy-dependent export mechanism encoded by the qacA gene. From nucleotide sequence analysis, qacA is predicted to encode a protein of Mr 55017 containing 514 amino acids. The gene is likely to initiate with a CUG codon, and a 36bp palindrome immediately preceding qacA, along with an upstream reading frame with homology to the TetR repressors, may be components of a regulatory circuit. The putative polypeptide specified by qacA has properties typical of a cytoplasmic membrane protein, and is indicated to be a member of a transport protein family that includes proteins reponsible for export-mediated resistance to tetracycline and methylenomycin, and uptake of sugars and quinate. The analysis suggests that N- and C-terminal regions of these proteins are involved in energy coupling (proton translocation) and substrate transport, respectively. The last common ancestor of the qacA and related tet (tetracycline resistance) lineages is inferred to have been repressor controlled, as occurs for modern tet determinants from Gram-negative, but not those from Gram-positive, bacteria.

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