scholarly journals OxyR2 Modulates OxyR1 Activity and Vibrio cholerae Oxidative Stress Response

2017 ◽  
Vol 85 (4) ◽  
Author(s):  
Hui Wang ◽  
Nawar Naseer ◽  
Yaran Chen ◽  
Anthony Y. Zhu ◽  
Xuewen Kuai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Vibrio Cholerae ◽  
Diarrheal Disease ◽  
Transcriptional Regulator ◽  
Cysteine Residue ◽  
Oxidative Stress Response ◽  
Human Pathogen ◽  
Content Type ◽  
Low Levels

ABSTRACT Bacteria have developed capacities to deal with different stresses and adapt to different environmental niches. The human pathogen Vibrio cholerae, the causative agent of the severe diarrheal disease cholera, utilizes the transcriptional regulator OxyR to activate genes related to oxidative stress resistance, including peroxiredoxin PrxA, in response to hydrogen peroxide. In this study, we identified another OxyR homolog in V. cholerae, which we named OxyR2, and we renamed the previous OxyR OxyR1. We found that OxyR2 is required to activate its divergently transcribed gene ahpC, encoding an alkylhydroperoxide reductase, independently of H2O2. A conserved cysteine residue in OxyR2 is critical for this function. Mutation of either oxyR2 or ahpC rendered V. cholerae more resistant to H2O2. RNA sequencing analyses indicated that OxyR1-activated oxidative stress-resistant genes were highly expressed in oxyR2 mutants even in the absence of H2O2. Further genetic analyses suggest that OxyR2-activated AhpC modulates OxyR1 activity by maintaining low intracellular concentrations of H2O2. Furthermore, we showed that ΔoxyR2 and ΔahpC mutants were less fit when anaerobically grown bacteria were exposed to low levels of H2O2 or incubated in seawater. These results suggest that OxyR2 and AhpC play important roles in the V. cholerae oxidative stress response.

scholarly journals Catalase Expression inAzospirillum brasilenseSp7 Is Regulated by a Network Consisting of OxyR and Two RpoH Paralogs and Including an RpoE1→RpoH5 Regulatory Cascade

2018 ◽  
Vol 84 (23) ◽  
Author(s):  
Ashutosh Kumar Rai ◽  
Sudhir Singh ◽  
Sushil Kumar Dwivedi ◽  
Amit Srivastava ◽  
Parul Pandey ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Sinorhizobium Meliloti ◽  
Deinococcus Radiodurans ◽  
Oxidative Stress Response ◽  
Sigma Factors ◽  
Transcriptional Analysis ◽  
Content Type ◽  
Regulatory Cascade ◽  
Transcription Regulators

ABSTRACTThe genome ofAzospirillum brasilenseencodes five RpoH sigma factors: two OxyR transcription regulators and three catalases. The aim of this study was to understand the role they play during oxidative stress and their regulatory interconnection. Out of the 5 paralogs of RpoH present inA. brasilense, inactivation of onlyrpoH1rendersA. brasilenseheat sensitive. While transcript levels ofrpoH1were elevated by heat stress, those ofrpoH3andrpoH5were upregulated by H2O2. Catalase activity was upregulated inA. brasilenseand itsrpoH::kmmutants in response to H2O2except in the case of therpoH5::kmmutant, suggesting a role for RpoH5 in regulating inducible catalase. Transcriptional analysis of thekatN,katAI, andkatAII genes revealed that the expression ofkatNandkatAII was severely compromised in therpoH3::kmandrpoH5::kmmutants, respectively. Regulation ofkatNandkatAII by RpoH3 and RpoH5, respectively, was further confirmed in anEscherichia colitwo-plasmid system. Regulation ofkatAII by OxyR2 was evident by a drastic reduction in growth, KatAII activity, andkatAII::lacZexpression in anoxyR2::kmmutant. This study reports the involvement of RpoH3 and RpoH5 sigma factors in regulating oxidative stress response in alphaproteobacteria. We also report the regulation of an inducible catalase by a cascade of alternative sigma factors and an OxyR. Out of the three catalases inA. brasilense, those corresponding tokatNandkatAII are regulated by RpoH3 and RpoH5, respectively. The expression ofkatAII is regulated by a cascade of RpoE1→RpoH5 and OxyR2.IMPORTANCEIn silicoanalysis of theA. brasilensegenome showed the presence of multiple paralogs of genes involved in oxidative stress response, which included 2 OxyR transcription regulators and 3 catalases. So far,Deinococcus radioduransandVibrio choleraeare known to harbor two paralogs of OxyR, andSinorhizobium melilotiharbors three catalases. We do not yet know how the expression of multiple catalases is regulated in any bacterium. Here we show the role of multiple RpoH sigma factors and OxyR in regulating the expression of multiple catalases inA. brasilenseSp7. Our work gives a glimpse of systems biology ofA. brasilenseused for responding to oxidative stress.

scholarly journals Nonthermal Plasma Induces the Viable-but-Nonculturable State in Staphylococcus aureus via Metabolic Suppression and the Oxidative Stress Response

2019 ◽  
Vol 86 (5) ◽  
Author(s):  
Xinyu Liao ◽  
Donghong Liu ◽  
Tian Ding
Keyword(s):  
Oxidative Stress ◽  
Staphylococcus Aureus ◽  
Stress Response ◽  
Nonthermal Plasma ◽  
Energy Allocation ◽  
Oxidative Stress Response ◽  
Vbnc State ◽  
Viable But Nonculturable ◽  
Content Type ◽  
Energy Dependent

ABSTRACT As a novel nonthermal technology, nonthermal plasma (NTP) has attracted a lot of attention. However, it could induce microorganisms into a viable but nonculturable (VBNC) state, posing a potential risk to food safety and public health. In this study, the molecular mechanisms of VBNC Staphylococcus aureus induced by NTP were investigated. With the use of a propidium monoazide quantitative PCR (PMA-qPCR) technique combined with a plate count method, we confirmed that 8.1 to 24.3 kJ NTP induced S. aureus into a VBNC state at a level of 7.4 to 7.6 log10 CFU/ml. The transcriptomic analysis was conducted and revealed that most energy-dependent physiological activities (e.g., metabolism) were arrested in VBNC S. aureus, while the oxidative stress response-related genes (katA, dps, msrB, msrA, and trxA) were significantly upregulated. In addition, this study showed that the ATP depletion by carbonyl cyanide m-chlorophenyl hydrazone (CCCP) pretreatment could accelerate the formation of VBNC S. aureus. The NTP-generated oxidative stress triggers the staphylococcal oxidative stress response, which consumes part of cellular energy (e.g., ATP). The energy allocation is therefore changed, and the energy assigned for other energy-dependent physiological activities (cell growth and division, etc.) is reduced, subsequently forcing S. aureus into a VBNC state. Therefore, the alterations of energy allocation should be some of the major contributors to the induction of VBNC S. aureus with NTP exposure. This study provides valuable knowledge for controlling the formation of VBNC S. aureus during NTP treatment. IMPORTANCE In recent years, nonthermal plasma (NTP) technology has received a lot of attention as a promising alternative to thermal pasteurization in the food industry. However, little is known about the microbial stress response toward NTP, which could be a potential risk to food safety and impede the development of NTP. A viable but nonculturable (VBNC) state is one of the most common survival strategies employed by microorganisms against external stress. This study investigated the mechanisms of the formation of VBNC Staphylococcus aureus by NTP in a more comprehensive and systematic aspect than had been done before. Our work confirmed that the NTP-generated oxidative stress induced changes in energy allocation as a driving force for the formation of VBNC S. aureus. This study could provide better knowledge for controlling the occurrence of VBNC S. aureus induced by NTP, which could lead to more rational design and ensure the development of safe foods.

scholarly journals Dps and DpsL Mediate SurvivalIn VitroandIn Vivoduring the Prolonged Oxidative Stress Response in Bacteroides fragilis

2015 ◽  
Vol 197 (20) ◽  
pp. 3329-3338 ◽  
Author(s):  
Michael I. Betteken ◽  
Edson R. Rocha ◽  
C. Jeffrey Smith
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Peritoneal Cavity ◽  
Bacteroides Fragilis ◽  
Oxidative Stress Response ◽  
Iron Storage ◽  
Content Type ◽  
Iron Storage Proteins

ABSTRACTBacteroides fragilisis a Gram-negative anaerobe and member of the human intestinal tract microbiome, where it plays many beneficial roles. However, translocation of the organism to the peritoneal cavity can lead to peritonitis, intra-abdominal abscess formation, bacteremia, and sepsis. During translocation,B. fragilisis exposed to increased oxidative stress from the oxygenated tissues of the peritoneal cavity and the immune response. In order to survive,B. fragilismounts a robust oxidative stress response consisting of an acute and a prolonged oxidative stress (POST) response. This report demonstrates that the ability to induce high levels of resistance totert-butyl hydroperoxide (tBOOH) after extended exposure to air can be linked to the POST response. Disk diffusion assays comparing the wild type to a Δdpsmutant and a ΔdpsΔbfrmutant showed greater sensitivity of the mutants to tBOOH after exposure to air, suggesting that Dps and DpsL play a role in the resistance phenotype. Complementation studies withdpsorbfr(encoding DpsL) restored tBOOH resistance, suggesting a role for both of these ferritin-family proteins in the response. Additionally, cultures treated with the iron chelator dipyridyl were not killed by tBOOH, indicating Dps and DpsL function by sequestering iron to prevent cellular damage. Anin vivoanimal model showed that the ΔdpsΔbfrmutant was attenuated, indicating that management of iron is important for survival within the abscess. Together, these data demonstrate a role for Dps and DpsL in the POST response which mediates survivalin vitroandin vivo.IMPORTANCEB. fragilisis the anaerobe most frequently isolated from extraintestinal opportunistic infections, but there is a paucity of information about the factors that allow this organism to survive outside its normal intestinal environment. This report demonstrates that the iron storage proteins Dps and DpsL protect against oxidative stress and that they contribute to survival bothin vitroandin vivo. Additionally, this work demonstrates an important role for the POST response inB. fragilissurvival and provides insight into the complex regulation of this response.

scholarly journals Necessity of OxyR for the Hydrogen Peroxide Stress Response and Full Virulence in Ralstonia solanacearum

2011 ◽  
Vol 77 (18) ◽  
pp. 6426-6432 ◽  
Author(s):  
Zomary Flores-Cruz ◽  
Caitilyn Allen
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Hydrogen Peroxide ◽  
Stress Response ◽  
Mutant Strain ◽  
Ralstonia Solanacearum ◽  
Oxidative Stress Response ◽  
Ros Scavenging ◽  
Content Type ◽  
Peroxide Stress

ABSTRACTThe plant pathogenRalstonia solanacearum, which causes bacterial wilt disease, is exposed to reactive oxygen species (ROS) during tomato infection and expresses diverse oxidative stress response (OSR) genes during midstage disease on tomato. TheR. solanacearumgenome predicts that the bacterium produces multiple and redundant ROS-scavenging enzymes but only one known oxidative stress response regulator, OxyR. AnR. solanacearumoxyRmutant had no detectable catalase activity, did not grow in the presence of 250 μM hydrogen peroxide, and grew poorly in the oxidative environment of solid rich media. This phenotype was rescued by the addition of exogenous catalase, suggesting thatoxyRis essential for the hydrogen peroxide stress response. Unexpectedly, theoxyRmutant strain grew better than the wild type in the presence of the superoxide generator paraquat. Gene expression studies indicated thatkatE,kaG,ahpC1,grxC, andoxyRitself were each differentially expressed in theoxyRmutant background and in response to hydrogen peroxide, suggesting thatoxyRis necessary for hydrogen peroxide-inducible gene expression. Additional OSR genes were differentially regulated in response to hydrogen peroxide alone. The virulence of theoxyRmutant strain was significantly reduced in both tomato and tobacco host plants, demonstrating thatR. solanacearumis exposed to inhibitory concentrations of ROSin plantaand that OxyR-mediated responses to ROS during plant pathogenesis are important forR. solanacearumhost adaptation and virulence.

scholarly journals Cyclo-(L-Phe-L-Pro), a Quorum-Sensing Signal ofVibrio vulnificus, Induces Expression of Hydroperoxidase through a ToxR-LeuO-HU-RpoS Signaling Pathway To Confer Resistance against Oxidative Stress

2018 ◽  
Vol 86 (9) ◽  
Author(s):  
In Hwang Kim ◽  
So-Yeon Kim ◽  
Na-Young Park ◽  
Yancheng Wen ◽  
Keun-Woo Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Virulence Factor ◽  
Vibrio Vulnificus ◽  
Transcriptional Regulator ◽  
Oxygen Species ◽  
Human Pathogen ◽  
Content Type ◽  
Opportunistic Human Pathogen ◽  
Bacterial Genes

ABSTRACTVibrio vulnificus, an opportunistic human pathogen, produces cyclo-(l-Phe-l-Pro) (cFP), which serves as a signaling molecule controlling the ToxR-dependent expression of innate bacterial genes, and also as a virulence factor eliciting pathogenic effects on human cells by enhancing intracellular reactive oxygen species levels. We found that cFP facilitated the protection ofV. vulnificusagainst hydrogen peroxide. At a concentration of 1 mM, cFP enhanced the level of the transcriptional regulator RpoS, which in turn induced expression ofkatG, encoding hydroperoxidase I, an enzyme that detoxifies H2O2to overcome oxidative stress. We found that cFP upregulated the transcription of the histone-like proteins vHUα and vHUβ through the cFP-dependent regulator LeuO. LeuO binds directly to upstream regions ofvhuAandvhuBto enhance transcription. vHUα and vHUβ then enhance the level of RpoS posttranscriptionally by stabilizing the mRNA. This cFP-mediated ToxR-LeuO-vHUαβ-RpoS pathway also upregulates genes known to be members of the RpoS regulon, suggesting that cFP acts as a cue for the signaling pathway responsible for both the RpoS and the LeuO regulons. Taken together, this study shows that cFP plays an important role as a virulence factor, as well as a signal for the protection of the cognate pathogen.

scholarly journals Genes Activated byVibrio choleraeupon Exposure toCaenorhabditis elegansReveal the Mannose-Sensitive Hemagglutinin To Be Essential for Colonization

mSphere ◽  
2018 ◽  
Vol 3 (3) ◽  
Author(s):  
Cornelia List ◽  
Andreas Grutsch ◽  
Claudia Radler ◽  
Fatih Cakar ◽  
Franz G. Zingl ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Vibrio Cholerae ◽  
Developmental Delay ◽  
Growth Retardation ◽  
Aquatic Environment ◽  
Diarrheal Disease ◽  
Phenotypic Characterization ◽  
Human Pathogen ◽  
Content Type ◽  
Human Host

ABSTRACTDuring its life cycle, the facultative human pathogenVibrio cholerae, which is the causative agent of the diarrheal disease cholera, needs to adapt to a variety of different conditions, such as the human host or the aquatic environment. Importantly, cholera infections originate from the aquatic reservoir whereV. choleraepersists between the outbreaks. In the aquatic environment, bacteria are constantly threatened by predatory protozoa and nematodes, but our knowledge of the response pathways and adaptation strategies ofV. choleraeto such stressors is limited. Using a temporally controlled reporter system of transcription, we identified more than 100 genes ofV. choleraeinduced upon exposure to the nematodeCaenorhabditis elegans, which emerged recently as a valuable model for environmental predation during the aquatic lifestyle ofV. cholerae. Besides others, we identified and validated the genes encoding the mannose-sensitive hemagglutinin (MSHA) type IV pilus to be significantly induced upon exposure to the nematode. Subsequent analyses demonstrated that the mannose-sensitive hemagglutinin is crucial for attachment ofV. choleraein the pharynx of the worm and initiation of colonization, which results in growth retardation and developmental delay ofC. elegans. Thus, the surface adhesion factor MSHA could be linked to a fitness advantage ofV. choleraeupon contact with bacterium-grazing nematodes.IMPORTANCEThe waterborne diarrheal disease cholera is caused by the bacteriumVibrio cholerae. The facultative human pathogen persists as a natural inhabitant in the aquatic ecosystem between outbreaks. In contrast to the human host,V. choleraerequires a different set of genes to survive in this hostile environment. For example, predatory micrograzers are commonly found in the aquatic environment and use bacteria as a nutrient source, but knowledge of the interaction between bacterivorous grazers andV. choleraeis limited. In this study, we successfully adapted a genetic reporter technology and identified more than 100 genes activated byV. choleraeupon exposure to the bacterium-grazing nematodeCaenorhabditis elegans. This screen provides a first glimpse into responses and adaptational strategies of the bacterial pathogen against such natural predators. Subsequent phenotypic characterization revealed the mannose-sensitive hemagglutinin to be crucial for colonization of the worm, which causes developmental delay and growth retardation.

scholarly journals A Point Mutation in the Transcriptional Repressor PerR Results in a Constitutive Oxidative Stress Response in Clostridioides difficile 630Δerm

mSphere ◽  
2021 ◽  
Vol 6 (2) ◽  
Author(s):  
Daniel Troitzsch ◽  
Hao Zhang ◽  
Silvia Dittmann ◽  
Dorothee Düsterhöft ◽  
Timon Alexander Möller ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Reference Strain ◽  
Transcriptional Repressor ◽  
Oxidative Stress Response ◽  
Detailed Knowledge ◽  
Single Nucleotide ◽  
Content Type ◽  
Clostridioides Difficile ◽  
Model Strain

ABSTRACT The human pathogen Clostridioides difficile has evolved into the leading cause of nosocomial diarrhea. The bacterium is capable of spore formation, which even allows survival of antibiotic treatment. Although C. difficile features an anaerobic lifestyle, we determined a remarkably high oxygen tolerance of the laboratory reference strain 630Δerm. A mutation of a single nucleotide (single nucleotide polymorphism [SNP]) in the DNA sequence (A to G) of the gene encoding the regulatory protein PerR results in an amino acid substitution (Thr to Ala) in one of the helices of the helix-turn-helix DNA binding domain of this transcriptional repressor in C. difficile 630Δerm. PerR is a sensor protein for hydrogen peroxide and controls the expression of genes involved in the oxidative stress response. We show that PerR of C. difficile 630Δerm has lost its ability to bind the promoter region of PerR-controlled genes. This results in a constitutive derepression of genes encoding oxidative stress proteins such as a rubrerythrin (rbr1) whose mRNA abundance under anaerobic conditions was increased by a factor of about 7 compared to its parental strain C. difficile 630. Rubrerythrin repression in strain 630Δerm could be restored by the introduction of PerR from strain 630. The permanent oxidative stress response of C. difficile 630Δerm observed here should be considered in physiological and pathophysiological investigations based on this widely used model strain. IMPORTANCE The intestinal pathogen Clostridioides difficile is one of the major challenges in medical facilities nowadays. In order to better combat the bacterium, detailed knowledge of its physiology is mandatory. C. difficile strain 630Δerm was generated in a laboratory from the patient-isolated strain C. difficile 630 and represents a reference strain for many researchers in the field, serving as the basis for the construction of insertional gene knockout mutants. In our work, we demonstrate that this strain is characterized by an uncontrolled oxidative stress response as a result of a single-base-pair substitution in the sequence of a transcriptional regulator. C. difficile researchers working with model strain 630Δerm should be aware of this permanent stress response.

scholarly journals Transcriptional Landscape and Regulatory Roles of Small Noncoding RNAs in the Oxidative Stress Response of the HaloarchaeonHaloferax volcanii

2018 ◽  
Vol 200 (9) ◽  
Author(s):  
Diego Rivera Gelsinger ◽  
Jocelyne DiRuggiero
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Environmental Conditions ◽  
Noncoding Rnas ◽  
Oxidative Stress Response ◽  
Haloferax Volcanii ◽  
Peptidase Activity ◽  
Content Type ◽  
Functional Roles ◽  
Transcriptional Landscape

ABSTRACTHaloarchaea in their natural environment are exposed to hypersalinity, intense solar radiation, and desiccation, all of which generate high levels of oxidative stress. Previous work has shown that haloarchaea are an order of magnitude more resistant to oxidative stress than most mesophilic organisms. Despite this resistance, the pathways haloarchaea use to respond to oxidative stress damage are similar to those of nonresistant organisms, suggesting that regulatory processes might be key to their robustness. Recently, small regulatory noncoding RNAs (sRNAs) were discovered inArchaeaunder a variety of environmental conditions. We report here the transcriptional landscape and functional roles of sRNAs in the regulation of the oxidative stress response of the model haloarchaeonHaloferax volcanii. Thousands of sRNAs, both intergenic and antisense, were discovered using strand-specific sRNA sequencing (sRNA-seq), comprising 25 to 30% of the total transcriptome under no-challenge and oxidative stress conditions, respectively. We identified hundreds of differentially expressed sRNAs in response to hydrogen peroxide-induced oxidative stress inH. volcanii. The targets of a group of antisense sRNAs decreased in expression when these sRNAs were upregulated, suggesting that sRNAs are potentially playing a negative regulatory role on mRNA targets at the transcript level. Target enrichment of these antisense sRNAs included mRNAs involved in transposon mobility, chemotaxis signaling, peptidase activity, and transcription factors.IMPORTANCEWhile a substantial body of experimental work has been done to uncover the functions of small regulatory noncoding RNAs (sRNAs) in gene regulation inBacteriaandEukarya, the functional roles of sRNAs inArchaeaare still poorly understood. This study is the first to establish the regulatory effects of sRNAs on mRNAs during the oxidative stress response in the haloarchaeonHaloferax volcanii. Our work demonstrates that common principles for the response to a major cellular stress exist across the 3 domains of life while uncovering pathways that might be specific to theArchaea. This work also underscores the relevance of sRNAs in adaptation to extreme environmental conditions.

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