The response of Staphylococcus aureus to hypochlorous acid (HOCl) exposure was investigated. HOCl challenges were performed on cultures interrupted in the exponential phase. Pretreatment with HOCl conferred resistance to hydrogen peroxide in a PerR-dependent manner. Derepression of the PerR regulon was observed at low HOCl concentration (survival >50 %), using several fusions of different stress promoters to lacZ reporter genes. At least four members of the PerR regulon (katA, mrgA, bcp and trxA) encoding proteins with antioxidant properties were strongly induced following exposure to various HOCl concentrations. A striking result was the link between the derepression of the PerR regulon and the decreased superoxide dismutase (SOD) activity following exposure to increased HOCl concentrations. The sodA mutant was more resistant than the wild-type and also had a higher level of 3-phosphoglycerate dehydrogenase (a measure of PerR regulon activity) without exposure to HOCl. Together, these results imply that derepression of PerR by HOCl is dependent on the level of SOD and protects exponentially arrested cells against HOCl stress.
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http://dx.doi.org/10.1099/mic.0.28385-0 | DOI Listing |
Mol Biotechnol
September 2024
School of Biotechnology, Jawaharlal Nehru University, New Delhi, 110067, India.
Bacteria have to thrive in difficult conditions wherein their competitors generate partially reduced forms of oxygen, like hydrogen peroxide and superoxides. These oxidative stress molecules can also arise from within via the autoxidation of redox enzymes. To adapt to such conditions, bacteria express detox enzymes as well as repair proteins.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
June 2024
Systems and Synthetic Biology Division, Department of Biology and Biological Engineering, Chalmers University of Technology, Gothenburg SE-412 96, Sweden.
In bacteria, attenuation of protein-tyrosine phosphorylation occurs during oxidative stress. The main described mechanism behind this effect is the HO-triggered conversion of bacterial phospho-tyrosines to protein-bound 3,4-dihydroxyphenylalanine. This disrupts the bacterial tyrosine phosphorylation-based signaling network, which alters the bacterial polysaccharide biosynthesis.
View Article and Find Full Text PDFWater Res
August 2024
National Engineering Research Center for Urban Pollution Control, State Key Laboratory of Pollution Control and Resource Reuse, College of Environmental Science and Engineering, Tongji University, Shanghai 200092, China.
Iron (Fe0, Fe (II), and Fe (III)) has been previously documented to upregulate the expression of key genes, enhancing the production of volatile fatty acids (VFAs) to achieve waste/wastewater resource recovery. However, the precise mechanism by why iron influences gene expression remains unclear. This study applied iron-assisted fermentation systems to explore the behind enhancing mechanism by constructing regulon networks among genes, microbes, and transcription factors.
View Article and Find Full Text PDFMol Microbiol
June 2024
Department of Chemistry and Biochemistry, Kennesaw State University, Kennesaw, Georgia, USA.
Bacteria contain conserved mechanisms to control the intracellular levels of metal ions. Metalloregulatory transcription factors bind metal cations and play a central role in regulating gene expression of metal transporters. Often, these transcription factors regulate transcription by binding to a specific DNA sequence in the promoter region of target genes.
View Article and Find Full Text PDFAntioxidants (Basel)
March 2024
Department of Biology, Division of Natural and Exact Sciences, University of Guanajuato, Guanajuato 36050, Mexico.
The guanine oxidized (GO) system of , composed of the YtkD (MutT), MutM and MutY proteins, counteracts the cytotoxic and genotoxic effects of the oxidized nucleobase 8-OxoG. Here, we report that in growing cells, the genetic inactivation of GO system potentiated mutagenesis (HPM), and subsequent hyperresistance, contributes to the damaging effects of hydrogen peroxide (HO) (HPHR). The mechanism(s) that connect the accumulation of the mutagenic lesion 8-OxoG with the ability of to evolve and survive the noxious effects of oxidative stress were dissected.
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