scholarly journals PgRsp Is a Novel Redox-Sensing Transcription Regulator Essential for Porphyromonas gingivalis Virulence

2019 ◽  
Vol 7 (12) ◽  
pp. 623
Author(s):  
Michał Śmiga ◽  
Teresa Olczak
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Porphyromonas Gingivalis ◽  
Alternative Pathway ◽  
Redox Status ◽  
Oxidative Stress Response ◽  
Gene Encoding ◽  
Expression Of Genes ◽  
Genes Encoding ◽  
Redox Sensing

Porphyromonas gingivalis is one of the etiological agents of chronic periodontitis. Both heme and oxidative stress impact expression of genes responsible for its survival and virulence. Previously we showed that P. gingivalis ferric uptake regulator homolog affects expression of a gene encoding a putative Crp/Fnr superfamily member, termed P. gingivalis redox-sensing protein (PgRsp). Although PgRsp binds heme and shows the highest similarity to proteins assigned to the CooA family, it could be a member of a novel, separate family of proteins with unknown function. Expression of the pgrsp gene is autoregulated and iron/heme dependent. Genes encoding proteins engaged in the oxidative stress response were upregulated in the pgrsp mutant (TO11) strain compared with the wild-type strain. The TO11 strain showed higher biomass production, biofilm formation, and coaggregation ability with Tannerella forsythia and Prevotella intermedia. We suggest that PgRsp may regulate production of virulence factors, proteases, Hmu heme acquisition system, and FimA protein. Moreover, we observed growth retardation of the TO11 strain under oxidative conditions and decreased survival ability of the mutant cells inside macrophages. We conclude that PgRsp protein may play a role in the oxidative stress response using heme as a ligand for sensing changes in redox status, thus regulating the alternative pathway of the oxidative stress response alongside OxyR.

scholarly journals Global Regulatory Impact of ClpP Protease of Staphylococcus aureus on Regulons Involved in Virulence, Oxidative Stress Response, Autolysis, and DNA Repair

2006 ◽  
Vol 188 (16) ◽  
pp. 5783-5796 ◽  
Author(s):  
Antje Michel ◽  
Franziska Agerer ◽  
Christof R. Hauck ◽  
Mathias Herrmann ◽  
Joachim Ullrich ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Staphylococcus Aureus ◽  
Dna Repair ◽  
Stress Response ◽  
Oxidative Stress Response ◽  
Transcriptional Analysis ◽  
Expression Of Genes ◽  
Wide Range ◽  
Genes Encoding ◽  
Regulatory Impact

ABSTRACT Staphylococcus aureus is an important pathogen, causing a wide range of infections including sepsis, wound infections, pneumonia, and catheter-related infections. In several pathogens ClpP proteases were identified by in vivo expression technologies to be important for virulence. Clp proteolytic complexes are responsible for adaptation to multiple stresses by degrading accumulated and misfolded proteins. In this report clpP, encoding the proteolytic subunit of the ATP-dependent Clp protease, was deleted, and gene expression of ΔclpP was determined by global transcriptional analysis using DNA-microarray technology. The transcriptional profile reveals a strong regulatory impact of ClpP on the expression of genes encoding proteins that are involved in the pathogenicity of S. aureus and adaptation of the pathogen to several stresses. Expression of the agr system and agr-dependent extracellular virulence factors was diminished. Moreover, the loss of clpP leads to a complete transcriptional derepression of genes of the CtsR- and HrcA-controlled heat shock regulon and a partial derepression of genes involved in oxidative stress response, metal homeostasis, and SOS DNA repair controlled by PerR, Fur, MntR, and LexA. The levels of transcription of genes encoding proteins involved in adaptation to anaerobic conditions potentially regulated by an Fnr-like regulator were decreased. Furthermore, the expression of genes whose products are involved in autolysis was deregulated, leading to enhanced autolysis in the mutant. Our results indicate a strong impact of ClpP proteolytic activity on virulence, stress response, and physiology in S. aureus.

Reduced oxidative-stress response in red blood cells from p45NFE2-deficient mice

Blood ◽  
2001 ◽  
Vol 97 (7) ◽  
pp. 2151-2158 ◽  
Author(s):  
Jefferson Y. Chan ◽  
Mandy Kwong ◽  
Margaret Lo ◽  
Renee Emerson ◽  
Frans A. Kuypers
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Leucine Zipper ◽  
Oxidative Stress Response ◽  
Severe Thrombocytopenia ◽  
Basic Leucine Zipper ◽  
Mild Anemia ◽  
Expression Of Genes

Abstract p45NF-E2 is a member of the cap ‘n’ collar (CNC)-basic leucine zipper family of transcriptional activators that is expressed at high levels in various types of blood cells. Mice deficient in p45NF-E2 that were generated by gene targeting have high mortality from bleeding resulting from severe thrombocytopenia. Survivingp45nf-e2−/− adults have mild anemia characterized by hypochromic red blood cells (RBCs), reticulocytosis, and splenomegaly. Erythroid abnormalities inp45nf-e2−/− animals were previously attributed to stress erythropoiesis caused by chronic bleeding and, possibly, ineffective erythropoiesis. Previous studies suggested that CNC factors might play essential roles in regulating expression of genes that protect cells against oxidative stress. In this study, we found that p45NF-E2–deficient RBCs have increased levels of reactive oxygen species and an increased susceptibility to oxidative-stress–induced damage. Deformability of p45NF-E2–deficient RBCs was markedly reduced with oxidative stress, and mutant cells had a reduced life span. One possible reason for increased sensitivity to oxidative stress is that catalase levels were reduced in mutant RBCs. These findings suggest a role for p45NF-E2 in the oxidative-stress response in RBCs and indicate that p45NF-E2 deficiency contributes to the anemia inp45nf-e2−/− mice.

scholarly journals PecS Is a Global Regulator of the Symptomatic Phase in the Phytopathogenic Bacterium Erwinia chrysanthemi 3937

2008 ◽  
Vol 190 (22) ◽  
pp. 7508-7522 ◽  
Author(s):  
Florence Hommais ◽  
Christine Oger-Desfeux ◽  
Frédérique Van Gijsegem ◽  
Sandra Castang ◽  
Sandrine Ligori ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Oxidative Stress Response ◽  
Erwinia Chrysanthemi ◽  
Secretion Systems ◽  
Phytopathogenic Bacterium ◽  
Temporal Regulation ◽  
Wide Range ◽  
Genes Encoding ◽  
Asymptomatic Phase

ABSTRACT Pathogenicity of the enterobacterium Erwinia chrysanthemi (Dickeya dadantii), the causative agent of soft-rot disease in many plants, is a complex process involving several factors whose production is subject to temporal regulation during infection. PecS is a transcriptional regulator that controls production of various virulence factors. Here, we used microarray analysis to define the PecS regulon and demonstrated that PecS notably regulates a wide range of genes that could be linked to pathogenicity and to a group of genes concerned with evading host defenses. Among the targets are the genes encoding plant cell wall-degrading enzymes and secretion systems and the genes involved in flagellar biosynthesis, biosurfactant production, and the oxidative stress response, as well as genes encoding toxin-like factors such as NipE and hemolysin-coregulated proteins. In vitro experiments demonstrated that PecS interacts with the regulatory regions of five new targets: an oxidative stress response gene (ahpC), a biosurfactant synthesis gene (rhlA), and genes encoding exported proteins related to other plant-associated bacterial proteins (nipE, virK, and avrL). The pecS mutant provokes symptoms more rapidly and with more efficiency than the wild-type strain, indicating that PecS plays a critical role in the switch from the asymptomatic phase to the symptomatic phase. Based on this, we propose that the temporal regulation of the different groups of genes required for the asymptomatic phase and the symptomatic phase is, in part, the result of a gradual modulation of PecS activity triggered during infection in response to changes in environmental conditions emerging from the interaction between both partners.

scholarly journals Oxidative Stress Response of Aspergillus oryzae Induced by Hydrogen Peroxide and Menadione Sodium Bisulfite

2019 ◽  
Vol 7 (8) ◽  
pp. 225 ◽  
Author(s):  
Shao ◽  
Tu ◽  
Wang ◽  
Jiang ◽  
Ma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Stress Response ◽  
Aspergillus Oryzae ◽  
Oxidative Stress Response ◽  
Sodium Bisulfite ◽  
Cellular Growth ◽  
Expression Of Genes ◽  
Menadione Sodium Bisulfite ◽  
Regulated Expression

Oxidative stress response protects organisms from deleterious effects of reactive oxygen species (ROS), which can damage cellular components and cause disturbance of the cellular homeostasis. Although the defensive biochemical mechanisms have been extensively studied in yeast and other filamentous fungi, little information is available about Aspergillus oryzae. We investigated the effect of two oxidant agents (menadione sodium bisulfite, MSB, and hydrogen peroxide, H2O2) on cellular growth and antioxidant enzyme induction in A. oryzae. Results indicated severe inhibition of biomass and conidia production when high concentration of oxidants was used. Transcriptomic analysis showed an up-regulated expression of genes involved in oxidoreduction, such as catalase, glutathione peroxidase, and superoxide dismutase. In addition, it was observed that oxidative stress stimuli enhanced the expression of Yap1 and Skn7 transcription factors. Further, metabolomic analysis showed that glutathione content was increased in the oxidative treatments when compared with the control. Moreover, the content of unsaturated fatty acid decreased with oxidative treatment accompanying with the down-regulated expression of genes involved in linoleic acid biosynthesis. This study provided a global transcriptome characterization of oxidative stress response in A. oryzae, and can offer multiple target genes for oxidative tolerance improvement via genetic engineering.

scholarly journals Energetic Consequences of Nitrite Stress in Desulfovibrio vulgaris Hildenborough, Inferred from Global Transcriptional Analysis

2006 ◽  
Vol 72 (6) ◽  
pp. 4370-4381 ◽  
Author(s):  
Qiang He ◽  
Katherine H. Huang ◽  
Zhili He ◽  
Eric J. Alm ◽  
Matthew W. Fields ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Iron Homeostasis ◽  
Oxidative Stress Response ◽  
Nitrite Reduction ◽  
Transcriptional Analysis ◽  
Cell Physiology ◽  
Desulfovibrio Vulgaris ◽  
Genes Encoding ◽  
Stressed Cells

ABSTRACT Many of the proteins that are candidates for bioenergetic pathways involved with sulfate respiration in Desulfovibrio spp. have been studied, but complete pathways and overall cell physiology remain to be resolved for many environmentally relevant conditions. In order to understand the metabolism of these microorganisms under adverse environmental conditions for improved bioremediation efforts, Desulfovibrio vulgaris Hildenborough was used as a model organism to study stress response to nitrite, an important intermediate in the nitrogen cycle. Previous physiological studies demonstrated that growth was inhibited by nitrite and that nitrite reduction was observed to be the primary mechanism of detoxification. Global transcriptional profiling with whole-genome microarrays revealed coordinated cascades of responses to nitrite in pathways of energy metabolism, nitrogen metabolism, oxidative stress response, and iron homeostasis. In agreement with previous observations, nitrite-stressed cells showed a decrease in the expression of genes encoding sulfate reduction functions in addition to respiratory oxidative phosphorylation and ATP synthase activity. Consequently, the stressed cells had decreased expression of the genes encoding ATP-dependent amino acid transporters and proteins involved in translation. Other genes up-regulated in response to nitrite include the genes in the Fur regulon, which is suggested to be involved in iron homeostasis, and genes in the Per regulon, which is predicted to be responsible for oxidative stress response.

scholarly journals A randomized observational analysis examining the correlation between patients’ food sensitivities, micronutrient deficiencies, oxidative stress response and immune redox status

2020 ◽  
Vol 10 (3) ◽  
pp. 143
Author(s):  
Irena Steele ◽  
Daniel Allright ◽  
Roger Deutsch
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Nutrient Deficiency ◽  
Redox Status ◽  
Oxidative Stress Response ◽  
Immune Reactivity ◽  
Micronutrient Deficiencies ◽  
Immune Functions ◽  
Food Sensitivity ◽  
Food Antigens

Background: Malnutrition due to insufficient intake of micronutrients, or due to impaired delivery of micronutrients to patients’ cells, is suppressing immune functions that are fundamental to host protection. Concurrently, an excessive triggering of patients’ immune reactions as the result of adverse responses to certain food antigens, can also lead to various chronic health conditions.Objective: To examine nutritional and immunological status in patients’ groups varying in age, dietary regimens and gastrointestinal condition; and explore a possible correlation between an impaired patients’ immune status and micronutrient deficiencies, food sensitivity and oxidative stress responses.Methods: This is a population-based study consisting of a American residents, age 13 and older, who completed the investigator’s provided questionnaires with application of cell-based individualized functional assays. Data for this paper were collected from 845 individuals between May and September 2019, as part of CSS CNA beta study. Micronutrient deficiencies, immune Redox status, antioxidative responses and food sensitivity profiles were assessed for each patient participating in this study.Results: The group of patients with low Redox status demonstrated significantly higher percent of immune reactivity (17%) to food antigens as compared to15% reactivity detected in the groups with the average and strong Redox response. An average number of identified micronutrient deficiencies, as well as beneficial anti-oxidative protective compounds, was also significantly higher in the group with the weak immune function as compared to other two groups.Conclusion: This study suggests that high food sensitivity is associated with a higher nutrient deficiency, a stronger oxidative stress response and a lower immune redox status. 

scholarly journals Identification of the Clostridium perfringens Genes Involved in the Adaptive Response to Oxidative Stress

2002 ◽  
Vol 184 (9) ◽  
pp. 2333-2343 ◽  
Author(s):  
V. Briolat ◽  
G. Reysset
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Clostridium Perfringens ◽  
Adaptive Response ◽  
Insertional Mutagenesis ◽  
Redox Balance ◽  
Single Copy ◽  
Oxidative Stress Response ◽  
Strictly Anaerobic ◽  
Gene Encoding

ABSTRACT Clostridium perfringens is a ubiquitous gram-positive pathogen that is present in the air, soil, animals, and humans. Although C. perfringens is strictly anaerobic, vegetative and stationary cells can survive in a growth-arrested stage in the presence of oxygen and/or low concentrations of superoxide and hydroxyl radicals. Indeed, it possesses an adaptive response to oxidative stress, which can be activated in both aerobic and anaerobic conditions. To identify the genes involved in this oxidative stress response, C. perfringens strain 13 mutants were generated by Tn916 insertional mutagenesis and screened for resistance or sensitivity to various oxidative stresses. Three of the 12 sensitive mutants examined harbored an independently inserted single copy of the transposon in the same operon as two genes orthologous to the ydaD and ycdF genes of Bacillus subtilis, which encode a putative NADPH dehydrogenase. Complementation experiments and knockout experiments demonstrated that these genes are both required for efficient resistance to oxidative stress in C. perfringens and are probably responsible for the production of NADPH, which is required for maintenance of the intracellular redox balance in growth-arrested cells. Other Tn916 disrupted genes were also shown to play important roles in the oxidative stress response. This is the first time that some of these genes (e.g., a gene encoding an ATP-dependent RNA helicase, the β-glucuronidase gene, and the gene encoding the atypical iron sulfur prismane protein) have been shown to be involved in the oxidative response.

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