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Changes in relative transcript amounts caused by hydrogen sulfide treatment, deletion of BigR, and BigR mutant complement in Acinetobacter baumannii

ABSTRACT: Acinetobacter baumannii is an opportunistic nosocomial pathogen that is the causative agent of several serious infections in humans. Here, we investigate the response of A. baumannii toward sodium sulfide (Na2S), known to be associated with some biofilms at oxic/anoxic interfaces, as a model for how this major human pathogen manages sulfide homeostasis. These results reveal that A. baumannii encodes two persulfide‑sensing transcriptional regulators, a primary sigma54‑dependent transcriptional activator (FisR), and a secondary system controlled by the persulfide‑sensing repressor biofilm growth‑associated repressor (BigR) both of which regulate operons encoding for sulfide detoxification or transportation. In addition, sulfide induces an alternative cytochrome bd oxidase which is refractory to inhibition by H2S and represses importers of alternate sulfur sources. Lastly, our results suggest additional genes regulated by BigR beyond sulfide detoxification including genes associated with assembly of type 1 chaperone-usher pilus.

ORGANISM(S): Acinetobacter baumannii

PROVIDER: GSE148264 | GEO | 2020/06/15

REPOSITORIES: GEO

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