Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1169012 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Revisiting oxygen toxicity: evolution and adaptation to superoxide in a SOD-deficient bacterial pathogen
| PRJNA1167678 | ENA
Project description:Revisiting oxygen toxicity: evolution and adaptation to superoxide in a SOD-deficient bacterial pathogen [paraquat]
| PRJNA1167677 | ENA
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 | GSE278514 | GEO
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
Project description:CuZn-superoxide dismutase (CuZn-SOD) and ascorbate peroxidase (APX) constitute first line of defence against oxidative stress. In the present study, PaSOD and RaAPX genes from Potentilla atrosanguinea and Rheum australe, respectively were overexpressed individually as well as in combination in Arabidopsis thaliana. We performed RNA-seq analysis of wild type and transgenic Arabidopsis thaliana overexpressing CuZn-SOD, APX and CuZn-SOD + APX under control and salt stress
2014-10-06 | E-MTAB-4434 | biostudies-arrayexpress
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
Project description:Plasmids are extrachromosomal genetic elements commonly found in bacteria. Plasmids are known to fuel bacterial evolution through horizontal gene transfer (HGT), but recent analyses indicate that they can also promote intragenomic adaptations. However, the role of plasmids as catalysts of bacterial evolution beyond HGT remains poorly explored. In this study, we investigate the impact of a widespread conjugative plasmid, pOXA-48, on the evolution of various multidrug-resistant clinical enterobacteria. Combining experimental and within-patient evolution analyses, we unveil that plasmid pOXA-48 promotes bacterial evolution through the transposition of plasmid-encoded IS1 elements. Specifically, IS1-mediated gene inactivations expedite the adaptation rate of clinical strains in vitro and foster within-patient adaptation in the gut. We decipher the mechanism underlying the plasmid-mediated surge in IS1 transposition, revealing a negative feedback loop regulated by the genomic copy number of IS1. Given the overrepresentation of IS elements in bacterial plasmids, our findings propose that plasmid-mediated IS transposition represents a crucial mechanism for swift bacterial adaptation.
2024-07-16 | GSE255663 | GEO
Project description:The Gram-negative photoheterotrophic bacterium Dinoroseobacter shibae is a member of the high abundant marine Roseobacter group. Living in the photic zone environment of marine ecosystems D. shibae is frequently exposed to oxygen. Oxic environments are hazardous and therefore effective defense mechanisms are required. In the present study, the adaptation of D. shibae to different kinds of oxidative stresses was investigated. Hydrogen peroxide, diamide and paraquat were used as agents to trigger peroxide, thiol and superoxide stress. To define and compare the peroxide, superoxide and thiol stress stimulons in D. shibae, GeLC-MS/MS based proteomic data of cytosolic and surface associated proteins were used. Furthermore, a strain deficient in the rhizobial iron regulator (RirA) was used to study the global impact of RirA on peroxide dependent protein expression.
2021-03-12 | PXD013791 | Pride
Project description:To investigate the pathological significance of excess oxidative stress in the heart, we generated heart/muscle-specific manganese superoxide dismutase (MnSOD) -deficient mice on a C57BL/6 background using the Cre-loxP system uder the control of the muscle reatin kinase (MCK) promoter. The mutant mice developed progressive congestive heart failure with dilated cardiomyopathy and physical disability and died with a median survival rate of 15.4 ± 4.0 weeks. The pathological changes in our model were compatible with human cardiac aging. To investigate the transcriptional alterations in the mutant heart, we carried out an Affymetrix microarray analysis for comparison between the mutant and normal heart at 16 weeks of age. Keywords = Mn-SOD Keywords = manganese superoxide dismutase Keywords = knockout Keywords = heart failure Keywords = heart Keywords = muscle Keywords: parallel sample
2005-02-05 | GSE2236 | GEO
Project description:Superoxide dismutases (SOD) convert superoxide to hydrogen peroxide and therefore provide an important ROS defence mechanism. SOD2 is the sole superoxide dismutase in mitochondrial matrix and thus SOD2 knockout mice can be utilized to analyse what effects increased oxidative stress has on mitochondrial proteome. To this end, we purified heart mitochondria from heart Sod2 knockout mice (Sod2 Ckmm cre) and controls and analysed their proteome with label free LS MS/MS.
2018-06-06 | PXD008998 | Pride