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. 2015 Apr 14;6:305. doi: 10.3389/fmicb.2015.00305

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Copyright © 2015 Podnecky, Rhodes and Schweizer.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The transcriptional regulator BpeT and locations of mutations causing multidrug resistance due to BpeEF-OprC expression. The figure illustrates the cause of BpeEF-OprC expression leading to a multidrug resistance phenotype due to bpeT mutations by comparing a prototype strain, in this instance a primary melioidosis isolate (strain 354b; Top), and a relapse isolate (strain 354e; Bottom). Strain 354b (Top) expresses wild-type BpeT that exhibits the typical LysR-type regular organization with an amino-terminal helix-turn-helix (HTH) DNA-binding domain and a co-inducer binding site located within the carboxy-terminal half. Point mutations located within the latter domain result in constitutive BpeEF-OprC eﬄux pump expression. Strain 354e (Bottom) expresses BpeEF-OprC constitutively due to deletion of the last 14 native bpeT codons as a consequence of a 800 kb inversion affecting chromosome 2 (Hayden et al., 2012).