scholarly journals Adaptation of Dinoroseobacter shibae to oxidative stress and the specific role of RirA

PLoS ONE ◽  
2021 ◽  
Vol 16 (3) ◽  
pp. e0248865
Author(s):  
Nicole Beier ◽  
Martin Kucklick ◽  
Stephan Fuchs ◽  
Ayten Mustafayeva ◽  
Maren Behringer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Resistance ◽  
Sole Carbon Source ◽  
Deletion Mutant ◽  
Iron Transport ◽  
Dinoroseobacter Shibae ◽  
Iron Binding Proteins ◽  
Peroxide Stress ◽  
Seawater Medium

Dinoroseobacter shibae living in the photic zone of marine ecosystems is frequently exposed to oxygen that forms highly reactive species. Here, we analysed the adaptation of D. shibae to different kinds of oxidative stress using a GeLC-MS/MS approach. D. shibae was grown in artificial seawater medium in the dark with succinate as sole carbon source and exposed to hydrogen peroxide, paraquat or diamide. We quantified 2580 D. shibae proteins. 75 proteins changed significantly in response to peroxide stress, while 220 and 207 proteins were differently regulated by superoxide stress and thiol stress. As expected, proteins like thioredoxin and peroxiredoxin were among these proteins. In addition, proteins involved in bacteriochlophyll biosynthesis were repressed under disulfide and superoxide stress but not under peroxide stress. In contrast, proteins associated with iron transport accumulated in response to peroxide and superoxide stress. Interestingly, the iron-responsive regulator RirA in D. shibae was downregulated by all stressors. A rirA deletion mutant showed an improved adaptation to peroxide stress suggesting that RirA dependent proteins are associated with oxidative stress resistance. Altogether, 139 proteins were upregulated in the mutant strain. Among them are proteins associated with protection and repair of DNA and proteins (e. g. ClpB, Hsp20, RecA, and a thioredoxin like protein). Strikingly, most of the proteins involved in iron metabolism such as iron binding proteins and transporters were not part of the upregulated proteins. In fact, rirA deficient cells were lacking a peroxide dependent induction of these proteins that may also contribute to a higher cell viability under these conditions.

scholarly journals Role of rgsA in Oxidative Stress Resistance in Pseudomonas aeruginosa

2021 ◽  
Author(s):  
Shuyi Hou ◽  
Jiaqin Zhang ◽  
Xiaobo Ma ◽  
Qiang Hong ◽  
Lili Fang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pseudomonas Aeruginosa ◽  
Stress Resistance ◽  
Oxidative Stress Resistance

scholarly journals Role of AccMGST1 in oxidative stress resistance in Apis cerana cerana

2019 ◽  
Vol 24 (4) ◽  
pp. 793-805 ◽  
Author(s):  
Wenchun Zhao ◽  
Yuzhen Chao ◽  
Ying Wang ◽  
Lijun Wang ◽  
Xinxin Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Resistance ◽  
Apis Cerana ◽  
Apis Cerana Cerana ◽  
Oxidative Stress Resistance

scholarly journals Role of the Filifactor alocis Hypothetical Protein FA519 in Oxidative Stress Resistance

2021 ◽  
Author(s):  
Ezinne Aja ◽  
Arunima Mishra ◽  
Yuetan Dou ◽  
Hansel M. Fletcher
Keyword(s):  
Oxidative Stress ◽  
Periodontal Disease ◽  
Stress Resistance ◽  
Hypothetical Protein ◽  
Content Type ◽  
Genetic Tools ◽  
Oxidative Stress Resistance ◽  
Filifactor Alocis ◽  
Diagnostic Indicator

Filifactor alocis is an emerging member of the periodontal community and is now proposed to be a diagnostic indicator of periodontal disease. However, due to the lack of genetic tools available to study this organism, not much is known about its virulence attributes.

Autophagy of iron-binding proteins may contribute to the oxidative stress resistance of ARPE-19 cells

2013 ◽  
Vol 116 ◽  
pp. 359-365 ◽  
Author(s):  
Markus Karlsson ◽  
Christina Frennesson ◽  
Therese Gustafsson ◽  
Ulf T. Brunk ◽  
Sven Erik G. Nilsson ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Resistance ◽  
Binding Proteins ◽  
Iron Binding ◽  
Oxidative Stress Resistance ◽  
Iron Binding Proteins

scholarly journals Autolysosomal degradation of cytosolic chromatin fragments antagonizes oxidative stress–induced senescence

2020 ◽  
Vol 295 (14) ◽  
pp. 4451-4463 ◽  
Author(s):  
Xiaojuan Han ◽  
Honghan Chen ◽  
Hui Gong ◽  
Xiaoqiang Tang ◽  
Ning Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Cellular Senescence ◽  
Bafilomycin A1 ◽  
Nih3t3 Cells ◽  
Present Evidence ◽  
Chromatin Fragment ◽  
Secretory Phenotype ◽  
Peroxide Stress

Oxidative stress-induced DNA damage, the senescence-associated secretory phenotype (SASP), and impaired autophagy all are general features of senescent cells. However, the cross-talk among these events and processes is not fully understood. Here, using NIH3T3 cells exposed to hydrogen peroxide stress, we show that stress-induced DNA damage provokes the SASP largely via cytosolic chromatin fragment (CCF) formation, which activates a cascade comprising cGMP-AMP synthase (cGAS), stimulator of interferon genes protein (STING), NF-κB, and SASP, and that autolysosomal function inhibits this cascade. We found that CCFs accumulate in senescent cells with activated cGAS-STING-NF-κB signaling, promoting SASP and cellular senescence. We also present evidence that the persistent accumulation of CCFs in prematurely senescent cells is partially associated with a defect in DNA-degrading activity in autolysosomes and reduced abundance of activated DNase 2α. Intriguingly, we found that metformin- or rapamycin-induced activation of autophagy significantly lessened the size and levels of CCFs and repressed the activation of the cGAS-STING-NF-κB-SASP cascade and cellular senescence. These effects of autophagy activators indicated that autolysosomal function contributes to CCF clearance and SASP suppression, further supported by the fact that the lysosome inhibitor bafilomycin A1 blocked the role of autophagy-mediated CCF clearance and senescence repression.

scholarly journals Contribution of the ATP-Dependent Protease ClpCP to the Autolysis and Virulence of Streptococcus pneumoniae

2005 ◽  
Vol 73 (2) ◽  
pp. 730-740 ◽  
Author(s):  
Yasser Musa Ibrahim ◽  
Alison R. Kerr ◽  
Nuno A. Silva ◽  
Tim J. Mitchell
Keyword(s):  
Oxidative Stress ◽  
Streptococcus Pneumoniae ◽  
Elevated Temperature ◽  
Stress Resistance ◽  
Pneumococcal Disease ◽  
Pathogenic Bacteria ◽  
Strain Dependent ◽  
Is Strain

ABSTRACT The ATP-dependent caseinolytic proteases (Clp) are fundamental for stress tolerance and virulence in many pathogenic bacteria. The role of ClpC in the autolysis and virulence of Streptococcus pneumoniae is controversial. In this study, we tested the role of ClpC in a number of S. pneumoniae strains and found that the contribution of ClpC to autolysis is strain dependent. ClpC is required for the release of autolysin A and pneumolysin in serotype 2 S. pneumoniae strain D39. In vivo, ClpC is required for the growth of the pneumococcus in the lungs and blood in a murine model of disease, but it does not affect the overall outcome of pneumococcal disease. We also report the requirement of ClpP for the growth at elevated temperature and virulence of serotype 4 strain TIGR4 and confirm its contribution to the thermotolerance, oxidative stress resistance, and virulence of D39.

The OxrA protein of Aspergillus fumigatus is required for the oxidative stress response and fungal pathogenesis

2021 ◽  
Author(s):  
Pengfei Zhai ◽  
Landan Shi ◽  
Guowei Zhong ◽  
Jihong Jiang ◽  
Jingwen Zhou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Immune Response ◽  
Stress Resistance ◽  
Pathogenic Fungi ◽  
Oxidative Stress Response ◽  
Fungal Pathogenesis ◽  
Oxygen Species ◽  
Oxidative Stress Resistance

An efficient reactive oxygen species (ROS) detoxification system is vital for the survival of the pathogenic fungus Aspergillus fumigatus within the host high ROS environment of the host. Therefore, identifying and targeting factors essential for oxidative stress response is one approach to develop novel treatments for fungal infections. Oxidation resistance 1 (Oxr1) protein is essential for protection against oxidative stress in mammals, but its functions in pathogenic fungi remain unknown. The present study aimed to characterize the role of an Oxr1 homolog in A. fumigatus . The results indicated that the OxrA protein plays an important role in oxidative stress resistance by regulating the catalase function in A. fumigatus , and overexpression of catalase can rescue the phenotype associated with OxrA deficiency. Importantly, the deficiency of oxrA decreased the virulence of A. fumigatus and altered the host immune response. Using the Aspergillus -induced lung infection model, we demonstrated that the ΔoxrA mutant strain induced less tissue damage along with decreased levels of LDH and albumin release. Additionally, the ΔoxrA mutant caused inflammation at a lower degree, along with a markedly reduced influx of neutrophils to the lungs and a decreased secretion of cytokine usually associated with recruitment of neutrophils in mice. These results characterize for the role of OxrA in A. fumigatus , as a core regulator of oxidative stress resistance and fungal pathogenesis. Importance Knowledge of reactive oxygen species (ROS) detoxification in fungal pathogens is useful in the design of new antifungal drugs and could aid in the study of oxidative stress resistance mechanisms. In this study, we demonstrate that OxrA protein localize to the mitochondria and function to protect against oxidative damage. We demonstrate that OxrA contributes to oxidative stress resistance by regulating catalase function, and overexpression of catalase (CatA or CatB) can rescue the phenotype that is associated with OxrA deficiency. Remarkably, a loss of OxrA attenuated the fungal virulence in a mouse model of invasive pulmonary aspergillosis and altered the host immune response. Therefore, our finding indicates that inhibition of OxrA might be an effective approach for alleviating A. fumigatus infection. The present study is, to the best of our knowledge, a pioneer in reporting the vital role of Oxr1 protein in pathogenic fungi.

scholarly journals Preventing Neurodegeneration by Controlling Oxidative Stress: The Role of OXR1

2020 ◽  
Vol 14 ◽  
Author(s):  
Michael R. Volkert ◽  
David J. Crowley
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Diseases ◽  
Stress Resistance ◽  
Molecular Level ◽  
Neuronal Damage ◽  
Gene Products ◽  
Oxidative Stress Resistance ◽  
Molecular Events ◽  
Regulatory Functions

Parkinson’s disease, diabetic retinopathy, hyperoxia induced retinopathy, and neuronal damage resulting from ischemia are among the notable neurodegenerative diseases in which oxidative stress occurs shortly before the onset of neurodegeneration. A shared feature of these diseases is the depletion of OXR1 (oxidation resistance 1) gene products shortly before the onset of neurodegeneration. In animal models of these diseases, restoration of OXR1 has been shown to reduce or eliminate the deleterious effects of oxidative stress induced cell death, delay the onset of symptoms, and reduce overall severity. Moreover, increasing OXR1 expression in cells further increases oxidative stress resistance and delays onset of disease while showing no detectable side effects. Thus, restoring or increasing OXR1 function shows promise as a therapeutic for multiple neurodegenerative diseases. This review examines the role of OXR1 in oxidative stress resistance and its impact on neurodegenerative diseases. We describe the potential of OXR1 as a therapeutic in light of our current understanding of its function at the cellular and molecular level and propose a possible cascade of molecular events linked to OXR1’s regulatory functions.

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