Genome-wide characterization of hypothiocyanite stress response of Escherichia coli reveals a potential role for RclB and RclC in lowering cell envelope permeability

Abstract

Oxidative stress is one of the major methods of microbial population control and pathogen clearing by the mammalian immune system. The methods by which bacteria are able to escape damage by host-derived oxidants such as hydrogen peroxide (H2O2) and hypochlorous acid (HOCl) have been relatively well described, while other oxidants effect on bacteria and their genetic responses are not as well understood. Hypothiocyanite/hypothiocyanous acid (-OSCN/HOSCN) is one such antimicrobial oxidant. In this study, we used RNA-sequencing to characterize the global transcriptional response of Escherichia coli to treatment with HOSCN and observed that the response is different from the responses of E. coli to other oxidants such as H2O2, superoxide, or HOCl, and distinct from the responses of other bacteria such as Streptococcus pneumoniae and Pseudomonas aeruginosa to HOSCN. Furthermore, we found that deletion of the genes encoded downstream of HOSCN reductase rclA in E. coli, rclB and rclC, has a transcriptional effect on ompC and may play a role in membrane permeability to HOSCN. IMPORTANCEUnderstanding how bacteria sense and respond to oxidative stress provides insights into how our bodies interact with the microbial population within us. In this study, we have characterized the genetic response of E. coli to important immune oxidant hypothiocyanite and investigated the role of the rclABC genes in that response.