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Steady-state hydrogen peroxide induces glycolysis via metabolic reroute in P. aeruginosa and S. aureus

ABSTRACT: Steady-state hydrogen peroxide induces glycolysis via metabolic reroute in P. aeruginosa and S. aureus

PROVIDER: PRJNA239877 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1182321.fastq.gz	Fastqsanger.gz
	SRR1182322.fastq.gz	Fastqsanger.gz
	SRR1182323.fastq.gz	Fastqsanger.gz
	SRR1182324.fastq.gz	Fastqsanger.gz
	SRR1182325.fastq.gz	Fastqsanger.gz

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Steady-state hydrogen peroxide induces glycolysis via metabolic reroute in P. aeruginosa and S. aureus

Project description:GAPDHs from human pathogens S. aureus and P. aeruginosa can be readily inhibited by ROS-mediated direct oxidation of their catalytic active cysteines. Because of the rapid degradation of H2O2 by bacterial catalase, only steady-state but not one-dose treatment of H2O2 induces rapid metabolic reroute from glycolysis to pentose phosphate pathway (PPP). We conducted RNA-seq analyses to globally profile the bacterial transcriptomes in response to a steady level of H2O2, which reveals profound transcriptional changes including the induced expression of glycolytic genes in both bacteria. Our results revealed that the inactivation of GAPDH by H2O2 induces a metabolic reroute from glycolysis to PPP; the elevated levels of fructose 1,6-biphosphate (FBP) and 2-keto-3-deoxy-6-phosphogluconate (KDPG) lead to dissociation of their corresponding glycolytic repressors (GapR and HexR, respectively) from their cognate promoters, thus resulting in derepression of the glycolytic genes to overcome H2O2-stalled glycolysis in S. aureus and P. aeruginosa, respectively. Given that H2O2 can be produced constitutively by the host immune response, exposure to the steady-state stress of H2O2 recapitulates more accurately bacterial responses to host immune system in vivo. RNA-seq in Pseudomonas aeruginosa and Staphylococus aureus under steady state of H2O2

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Steady-state hydrogen peroxide induces glycolysis via metabolic reroute in P. aeruginosa and S. aureus

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Project description:Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) from human pathogens Staphylococcus aureus and Pseudomonas aeruginosa can be readily inhibited by reactive oxygen species (ROS)-mediated direct oxidation of their catalytic active cysteines. Because of the rapid degradation of H2O2 by bacterial catalase, only steady-state but not one-dose treatment with H2O2 rapidly induces glycolysis and the pentose phosphate pathway (PPP). We conducted transcriptome sequencing (RNA-seq) analyses to globally profile the bacterial transcriptomes in response to a steady level of H2O2, which revealed profound transcriptional changes, including the induced expression of glycolytic genes in both bacteria. Our results revealed that the inactivation of GAPDH by H2O2 induces metabolic levels of glycolysis and the PPP; the elevated levels of fructose 1,6-biphosphate (FBP) and 2-keto-3-deoxy-6-phosphogluconate (KDPG) lead to dissociation of their corresponding glycolytic repressors (GapR and HexR, respectively) from their cognate promoters, thus resulting in derepression of the glycolytic genes to overcome H2O2-stalled glycolysis in S. aureus and P. aeruginosa, respectively. Both GapR and HexR may directly sense oxidative stresses, such as menadione.

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