The local repressor AcrR plays a modulating role in the regulation of <i>acrAB genes of Escherichia coli</i> by global stress signals

TLDR

The acrAB operon encodes a multidrug efflux pump whose transcription is up‑regulated by general stress conditions such as ethanol, high salt, or stationary phase, and this induction appears to be independent of the known regulators MarA and SoxS. The authors used lacZ transcriptional fusions and in‑vitro gel‑shift assays to dissect acrAB regulation. AcrR functions as a repressor of acrAB, and although stress conditions still elevate acrAB transcription without functional AcrR, they also strongly induce acrR itself, indicating that global stress pathways drive acrAB expression while AcrR fine‑tunes the response to prevent overexpression—a novel regulatory mechanism in *E.

Abstract

Summary Genes acrAB encode a multidrug efflux pump in Escherichia coli . We have previously reported that transcription of acrAB is increased under general stress conditions (i.e. 4% ethanol, 0.5 M NaCl, and the stationary phase in Luria‐Bertanl medium). In this study, lacZ transcriptional fusions and an in vitro gel mobility shift assay have been utilized to study the mechanisms governing the regulation of acrAB . We found that a closely linked gene, acrR , encoded a repressor of acrAB . Nevertheless, the general stress conditions increased transcription of acrAB in the absence of functional AcrR, and such conditions surprisingly increased the transcription of acrR even more strongly than that of acrAB . These results suggest that the general‐stress‐induced transcription of acrAB is primarily mediated by global regulatory pathway(s), and that one major role of AcrR is to function as a specific secondary modulator to fine tune the level of acrAB transcription and to prevent the unwanted overexpression of acrAB . To our knowledge, this represents a novel mechanism of regulating gene expression in E. coli . Evidence also suggests that the up‐regulation of acrAB expression under general stress conditions is not likely to be mediated by the known global regulators, such as MarA or SoxS, although elevated levels of these proteins were shown to increase the transcription of acrAB .