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Revisiting oxygen toxicity: evolution and adaptation to superoxide in a SOD-deficient bacterial pathogen

ABSTRACT: Revisiting oxygen toxicity: evolution and adaptation to superoxide in a SOD-deficient bacterial pathogen

PROVIDER: PRJNA1167678 | ENA |

REPOSITORIES: ENA

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Revisiting oxygen toxicity: evolution and adaptation to superoxide in a SOD-deficient bacterial pathogen

Project description:Defenses against oxidants are crucial for the virulence of pathogens, with superoxide scavenging enzymes (SOSEs) playing a vital role for most aerobes. However, our knowledge of superoxide adaptation primarily stems from the study of SOSE-encoding bacteria. Here, we investigated the evolution of a naturally SOSE-deficient pathogen (Leptospira spp.), along with the alternative mechanisms it recruits to combat superoxide stress. We demonstrate that emergence of pathogenic Leptospira correlated with SOD loss, but that a long-lasting adaptation to superoxide remains possible. We reveal that cysteine and leucine biosynthesis are the most induced pathways in response to superoxide and demonstrate the importance of sulfur metabolism in superoxide adaptation in this SOSE-deficient model. We also propose cysteine oxidation as a key mediator of superoxide toxicity in the absence of SOSEs. This study challenges our conventional understanding of the oxygen toxicity theory and proposes a new model of superoxide adaptation through metabolic rewiring in bacteria.

2025-07-15 | GSE278513 | GEO

Revisiting oxygen toxicity: evolution and adaptation to superoxide in a SOD-deficient bacterial pathogen [paraquat]

2025-07-15 | GSE278514 | GEO

Revisiting oxygen toxicity: evolution and adaptation to superoxide in a SOD-deficient bacterial pathogen [paraquat]

Project description:Revisiting oxygen toxicity: evolution and adaptation to superoxide in a SOD-deficient bacterial pathogen [paraquat]

| PRJNA1167677 | ENA

Molecular mechanisms of lifespan extension in long-lived mitocondrial superoxide dismutase sod-2 mutants

Project description:To explore the molecular mechanisms of lifespan extension in sod-2 mutants in an unbiased manner, we used RNA sequencing to identify differentially expressed genes in sod-2 mutants compared to wild-type worms. We found a large number of gene expression changes at day 1 of adulthood and much fewer at day 8. Upregulated genes in sod-2 mutants included genes involved in innate immunity and cuticle development. There were many more differentially expressed genes between day 1 and day 8 of adulthood compared to differences between the genotypes.

2025-02-25 | GSE286219 | GEO

Project description:Revisiting oxygen toxicity: evolution and adaptation to superoxide in a SOD-deficient bacterial pathogen

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Molecular mechanisms of lifespan extension in long-lived mitocondrial superoxide dismutase sod-2 mutants

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Redistribution of EC-SOD due to the R213G SNP reveals differential RNA-seq profile of recruited alveolar macrophages and accelerated apoptosis in response to bleomycin

Project description:A known human SNP in the matrix-binding domain of extracellular superoxide dismutase (EC-SOD), with an arginine to glycine substitution at position 213 (R213G), redistributes EC-SOD from the matrix into extracellular fluids. We reported that, following bleomycin (bleo), knock-in mice harboring the human R213G SNP (R213G mice), compared to wild-type (WT) littermates exhibit enhanced resolution of inflammation and protection against fibrosis. We tested the hypothesis that the EC-SOD R213G SNP promotes resolution via accelerated apoptosis of recruited alveolar macrophage (recAM).

2022-02-01 | GSE127345 | GEO

Superoxide dismutase SOD-1 modulates C. elegans pathogen avoidance behavior.

Project description:The C. elegans nervous system mediates protective physiological and behavioral responses amid infection. However, it remains largely unknown how the nervous system responds to reactive oxygen species (ROS) activated by pathogenic microbes during infection. Here, we show superoxide dismutase-1 (SOD-1), an enzyme that converts superoxide into less toxic hydrogen peroxide and oxygen, functions in the gustatory neuron ASER to mediate C. elegans pathogen avoidance response. When C. elegans first encounters pathogenic bacteria P. aeruginosa, SOD-1 is induced in the ASER neuron. After prolonged P. aeruginosa exposure, ASER-specific SOD-1 expression is diminished. In turn, C. elegans starts to vacate the pathogenic bacteria lawn. Genetic knockdown experiments reveal that pathogen-induced ROS activate sod-1 dependent behavioral response non cell-autonomously. We postulate that the delayed aversive response to detrimental microbes may provide survival benefits by allowing C. elegans to temporarily utilize food that is tainted with pathogens as an additional energy source. Our data offer a mechanistic insight into how the nervous system mediates food-seeking behavior amid oxidative stress and suggest that the internal state of redox homeostasis could underlie the behavioral response to harmful microbial species.

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Profiling wt SOD versus ALS SOD1(G93A) mutant

Project description:Whole-genome profiling of SH-SY5Y cells was done on neuroblastoma SH-SY5Y stably transfected with cDNAs coding for SOD1WT or the mutant SOD1(G93A) protein. Five wt SOD versus five mutant SOD

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Project description:Revisiting the putative role of heme as a trigger of inflammation

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