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Antibiotic resistance and oxidative stress response are important biological mechanisms that help bacteria thrive, especially pathogenic bacteria like Escherichia coli. Hydrogen sulfide (H 2 S), a chemical messenger molecule, regulates several intracellular activities in bacteria such as responses to oxidative stress and antibiotics.

Increased iron uptake triggered by intracellular H 2 S levels has been identified in the pathogenic bacterium Vibrio cholerae, contributing to its oxidative stress response. However, the precise mechanism behind H 2 S dependent cellular responses of E. coli remains unclear.

A team of researchers led by Professor Shinji Masuda from the Department of Life Science & Technology, Tokyo Institute of Technology, Japan have attempted to unravel the underlying mechanism and relationship between intracellular H 2 S and iron uptake in E. coli. They utilized a genetically manipulated wild-type (WT) E. coli strain overexpressing mstA, which encodes 3-mercaptopyruvate sulfur transferase enzyme responsible for the production of H 2 S.

Additionally, they employed advanced genetic sequencing techniques and assays to identify the molecular pathways involved in the overall regulation of iron uptake in response to H 2 S availability. Their findings were published in the mBio journal.

Sharing the motivation and rationale behind the present research, Masuda states, "Our research group had previously identified and characterized the arsenic repressor-type H 2 S-/supersulfide-responsive transcription factor SqrR in the purple photosynthetic bacterium Rhodobacter capsulatus, where SqrR regulated gene expression in response to H 2 S availability.

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