scholarly journals Metabolic Reprogramming ofVibrio choleraeImpaired in Respiratory NADH Oxidation Is Accompanied by Increased Copper Sensitivity

2018 ◽  
Vol 200 (15) ◽  
Author(s):  
Charlotte Toulouse ◽  
Kristina Metesch ◽  
Jens Pfannstiel ◽  
Julia Steuber
Keyword(s):  
Vibrio Cholerae ◽  
Pathogenic Bacteria ◽  
Carbon Sources ◽  
Copper Resistance ◽  
Metabolic Reprogramming ◽  
Deletion Strain ◽  
Substrate Uptake ◽  
Content Type ◽  
Nadh:Quinone Oxidoreductase ◽  
The Impact

ABSTRACTThe electrogenic, sodium ion-translocating NADH:quinone oxidoreductase (NQR) fromVibrio choleraeis frequent in pathogenic bacteria and a potential target for antibiotics. NQR couples the oxidation of NADH to the formation of a sodium motive force (SMF) and therefore drives important processes, such as flagellar rotation, substrate uptake, and energy-dissipating cation-proton antiport. We performed a quantitative proteome analysis ofV. choleraeO395N1 compared to its variant lacking the NQR using minimal medium with glucose as the carbon source. We found 84 proteins (regulation factor of ≥2) to be changed in abundance. The loss of NQR resulted in a decrease in the abundance of enzymes of the oxidative branch of the tricarboxylic acid (TCA) cycle and an increase in abundance of virulence factors AcfC and TcpA. Most unexpected, the copper resistance proteins CopA, CopG, and CueR were decreased in thenqrdeletion strain. As a consequence, the mutant exhibited diminished resistance to copper compared to the reference strain, as confirmed in growth studies using either glucose or mixed amino acids as carbon sources. We propose that the observed adaptations of thenqrdeletion strain represent a coordinated response which counteracts a drop in transmembrane voltage that challengesV. choleraein its different habitats.IMPORTANCEThe importance of the central metabolism for bacterial virulence has raised interest in studying catabolic enzymes not present in the host, such as NQR, as putative targets for antibiotics.Vibrio choleraelacking the NQR, which is studied here, is a model to estimate the impact of specific NQR inhibitors on the phenotype of a pathogen. Our comparative proteomic study provides a framework to evaluate the chances of success of compounds directed against NQR with respect to their bacteriostatic or bactericidal action.

scholarly journals Antibiotic Korormicin A Kills Bacteria by Producing Reactive Oxygen Species

2019 ◽  
Vol 201 (11) ◽  
Author(s):  
Adam Maynard ◽  
Nicole L. Butler ◽  
Takeshi Ito ◽  
Adilson José da Silva ◽  
Masatoshi Murai ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Pseudomonas Aeruginosa ◽  
Vibrio Cholerae ◽  
Pathogenic Bacteria ◽  
Reactive Oxygen ◽  
Direct Result ◽  
Oxygen Species ◽  
Gram Negative ◽  
Content Type ◽  
Nadh:Quinone Oxidoreductase

ABSTRACT Korormicin is an antibiotic produced by some pseudoalteromonads which selectively kills Gram-negative bacteria that express the Na+-pumping NADH:quinone oxidoreductase (Na+-NQR.) We show that although korormicin is an inhibitor of Na+-NQR, the antibiotic action is not a direct result of inhibiting enzyme activity. Instead, perturbation of electron transfer inside the enzyme promotes a reaction between O2 and one or more redox cofactors in the enzyme (likely the flavin adenine dinucleotide [FAD] and 2Fe-2S center), leading to the production of reactive oxygen species (ROS). All Pseudoalteromonas contain the nqr operon in their genomes, including Pseudoalteromonas strain J010, which produces korormicin. We present activity data indicating that this strain expresses an active Na+-NQR and that this enzyme is not susceptible to korormicin inhibition. On the basis of our DNA sequence data, we show that the Na+-NQR of Pseudoalteromonas J010 carries an amino acid substitution (NqrB-G141A; Vibrio cholerae numbering) that in other Na+-NQRs confers resistance against korormicin. This is likely the reason that a functional Na+-NQR is able to exist in a bacterium that produces a compound that typically inhibits this enzyme and causes cell death. Korormicin is an effective antibiotic against such pathogens as Vibrio cholerae, Aliivibrio fischeri, and Pseudomonas aeruginosa but has no effect on Bacteroides fragilis and Bacteroides thetaiotaomicron, microorganisms that are important members of the human intestinal microflora. IMPORTANCE As multidrug antibiotic resistance in pathogenic bacteria continues to rise, there is a critical need for novel antimicrobial agents. An essential requirement for a useful antibiotic is that it selectively targets bacteria without significant effects on the eukaryotic hosts. Korormicin is an excellent candidate in this respect because it targets a unique respiratory enzyme found only in prokaryotes, the Na+-pumping NADH:quinone oxidoreductase (Na+-NQR). Korormicin is synthesized by some species of the marine bacterium Pseudoalteromonas and is a potent and specific inhibitor of Na+-NQR, an enzyme that is essential for the survival and proliferation of many Gram-negative human pathogens, including Vibrio cholerae and Pseudomonas aeruginosa, among others. Here, we identified how korormicin selectively kills these bacteria. The binding of korormicin to Na+-NQR promotes the formation of reactive oxygen species generated by the reaction of the FAD and the 2Fe-2S center cofactors with O2.

scholarly journals Impact of Na+-Translocating NADH:Quinone Oxidoreductase on Iron Uptake and nqrM Expression in Vibrio cholerae

2019 ◽  
Vol 202 (3) ◽  
Author(s):  
Shubhangi Agarwal ◽  
Melanie Bernt ◽  
Charlotte Toulouse ◽  
Hannes Kurz ◽  
Jens Pfannstiel ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Iron Uptake ◽  
Iron Homeostasis ◽  
Mrna Level ◽  
Strong Impact ◽  
Substrate Uptake ◽  
Uptake System ◽  
Content Type ◽  
Respiratory Enzyme ◽  
Nadh:Quinone Oxidoreductase

ABSTRACT The Na+ ion-translocating NADH:quinone oxidoreductase (NQR) from Vibrio cholerae is a membrane-bound respiratory enzyme which harbors flavins and Fe-S clusters as redox centers. The NQR is the main producer of the sodium motive force (SMF) and drives energy-dissipating processes such as flagellar rotation, substrate uptake, ATP synthesis, and cation-proton antiport. The NQR requires for its maturation, in addition to the six structural genes nqrABCDEF, a flavin attachment gene, apbE, and the nqrM gene, presumably encoding a Fe delivery protein. We here describe growth studies and quantitative real-time PCR for the V. cholerae O395N1 wild-type (wt) strain and its mutant Δnqr and ΔubiC strains, impaired in respiration. In a comparative proteome analysis, FeoB, the membrane subunit of the uptake system for Fe2+ (Feo), was increased in V. cholerae Δnqr. In this study, the upregulation was confirmed on the mRNA level and resulted in improved growth rates of V. cholerae Δnqr with Fe2+ as an iron source. We studied the expression of feoB on other respiratory enzyme deletion mutants such as the ΔubiC mutant to determine whether iron transport is specific to the absence of NQR resulting from impaired respiration. We show that the nqr operon comprises, in addition to the structural nqrABCDEF genes, the downstream apbE and nqrM genes on the same operon and demonstrate induction of the nqr operon by iron in V. cholerae wt. In contrast, expression of the nqrM gene in V. cholerae Δnqr is repressed by iron. The lack of functional NQR has a strong impact on iron homeostasis in V. cholerae and demonstrates that central respiratory metabolism is interwoven with iron uptake and regulation. IMPORTANCE Investigating strategies of iron acquisition, storage, and delivery in Vibrio cholerae is a prerequisite to understand how this pathogen thrives in hostile, iron-limited environments such as the human host. In addition to highlighting the maturation of the respiratory complex NQR, this study points out the influence of NQR on iron metabolism, thereby making it a potential drug target for antibiotics.

scholarly journals The Na+-Translocating NADH:Quinone Oxidoreductase Enhances Oxidative Stress in the Cytoplasm of Vibrio cholerae

2016 ◽  
Vol 198 (17) ◽  
pp. 2307-2317 ◽  
Author(s):  
Valentin Muras ◽  
Paul Dogaru-Kinn ◽  
Yusuke Minato ◽  
Claudia C. Häse ◽  
Julia Steuber
Keyword(s):  
Reactive Oxygen Species ◽  
Vibrio Cholerae ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Content Type ◽  
Nadh:Quinone Oxidoreductase ◽  
Quinone Reduction ◽  
Superoxide Formation ◽  
The Impact

ABSTRACTWe searched for a source of reactive oxygen species (ROS) in the cytoplasm of the human pathogenVibrio choleraeand addressed the mechanism of ROS formation using the dye 2′,7′-dichlorofluorescein diacetate (DCFH-DA) in respiring cells. By comparingV. choleraestrains with or without active Na+-translocating NADH:quinone oxidoreductase (Na+-NQR), this respiratory sodium ion redox pump was identified as a producer of ROSin vivo. The amount of cytoplasmic ROS detected inV. choleraecells producing variants of Na+-NQR correlated well with rates of superoxide formation by the corresponding membrane fractions. Membranes from wild-typeV. choleraeshowed increased superoxide production activity (9.8 ± 0.6 μmol superoxide min−1mg−1membrane protein) compared to membranes from the mutant lacking Na+-NQR (0.18 ± 0.01 μmol min−1mg−1). Overexpression of plasmid-encoded Na+-NQR in thenqrdeletion strain resulted in a drastic increase in the formation of superoxide (42.6 ± 2.8 μmol min−1mg−1). By analyzing a variant of Na+-NQR devoid of quinone reduction activity, we identified the reduced flavin adenine dinucleotide (FAD) cofactor of cytoplasmic NqrF subunit as the site for intracellular superoxide formation inV. cholerae. The impact of superoxide formation by the Na+-NQR on the virulence ofV. choleraeis discussed.IMPORTANCEIn several studies, it was demonstrated that the Na+-NQR inV. choleraeaffects virulence in a yet unknown manner. We identified the reduced FAD cofactor in the NADH-oxidizing NqrF subunit of the Na+-NQR as the site of superoxide formation in the cytoplasm ofV. cholerae. Our study provides the framework to understand how reactive oxygen species formed during respiration could participate in the regulated expression of virulence factors during the transition from aerobic to microaerophilic (intestinal) habitats. This hypothesis may turn out to be right for many other pathogens which, likeV. cholerae, depend on the Na+-NQR as the sole electrogenic NADH dehydrogenase.

scholarly journals Evaluation of Whole-Genome Sequencing for Identification and Typing of Vibrio cholerae

2018 ◽  
Vol 56 (11) ◽  
Author(s):  
David R. Greig ◽  
Ulf Schaefer ◽  
Sophie Octavia ◽  
Ebony Hunter ◽  
Marie A. Chattaway ◽  
...  
Keyword(s):  
Public Health ◽  
Whole Genome Sequencing ◽  
Vibrio Cholerae ◽  
Species Identification ◽  
Genome Sequencing ◽  
National Level ◽  
Whole Genome ◽  
Content Type ◽  
El Tor ◽  
The Impact

ABSTRACT Epidemiological and microbiological data on Vibrio cholerae strains isolated between April 2004 and March 2018 (n = 836) and held at the Public Health England culture archive were reviewed. The traditional biochemical species identification and serological typing results were compared with the genome-derived species identification and serotype for a subset of isolates (n = 152). Of the 836 isolates, 750 (89.7%) were from a fecal specimen, 206 (24.6%) belonged to serogroup O1, and 7 (0.8%) were serogroup O139; 792 (94.7%) isolates were from patients reporting recent travel abroad, most commonly to India (n = 209) and Pakistan (n = 104). Of the 152 V. cholerae isolates identified by use of kmer, 149 (98.1%) were concordant with those identified using the traditional biochemical approach. Traditional serotyping results were 100% concordant with those of the whole-genome sequencing (WGS) analysis for the identification of serogroups O1 and O139 and classical and El Tor biotypes. ctxA was detected in all isolates of V. cholerae O1 El Tor and O139 belonging to sequence type 69 (ST69) and in V. cholerae O1 classical variants belonging to ST73. A phylogeny of isolates belonging to ST69 from U.K. travelers clustered geographically, with isolates from India and Pakistan located on separate branches. Moving forward, WGS data from U.K. travelers will contribute to global surveillance programs and the monitoring of emerging threats to public health and the global dissemination of pathogenic lineages. At the national level, these WGS data will inform the timely reinforcement of direct public health messaging to travelers and mitigate the impact of imported infections and the associated risks to public health.

scholarly journals Metabolic Reprogramming in the Opportunistic Yeast Candida albicans in Response to Hypoxia

mSphere ◽  
2020 ◽  
Vol 5 (1) ◽  
Author(s):  
Anaïs Burgain ◽  
Faiza Tebbji ◽  
Inès Khemiri ◽  
Adnane Sellam
Keyword(s):  
Cell Wall ◽  
Candida Albicans ◽  
Metabolic Pathways ◽  
Membrane Lipids ◽  
Oxygen Depletion ◽  
Metabolic Reprogramming ◽  
Pathogenic Yeast ◽  
Fungal Virulence ◽  
Content Type ◽  
The Impact

ABSTRACT Hypoxia is the predominant condition that the human opportunistic fungus Candida albicans encounters in the majority of the colonized niches within the host. So far, the impact of such a condition on the overall metabolism of this important human-pathogenic yeast has not been investigated. Here, we have undertaken a time-resolved metabolomics analysis to uncover the metabolic landscape of fungal cells experiencing hypoxia. Our data showed a dynamic reprogramming of many fundamental metabolic pathways, such as glycolysis, the pentose phosphate pathway, and different metabolic routes related to fungal cell wall biogenesis. The C. albicans lipidome was highly affected by oxygen depletion, with an increased level of free fatty acids and biochemical intermediates of membrane lipids, including phospholipids, lysophospholipids, sphingolipids, and mevalonate. The depletion of oxygen-dependent lipids such as ergosterol or phosphatidylcholine with longer and polyunsaturated lateral fatty acid chains was observed only at the later hypoxic time point (180 min). Transcriptomics data supported the main metabolic response to hypoxia when matched to our metabolomic profiles. The hypoxic metabolome reflected different physiological alterations of the cell wall and plasma membrane of C. albicans under an oxygen-limiting environment that were confirmed by different approaches. This study provided a framework for future in vivo investigations to examine relevant hypoxic metabolic trajectories in fungal virulence and fitness within the host. IMPORTANCE A critical aspect of cell fitness is the ability to sense and adapt to variations in oxygen levels in their local environment. Candida albicans is an opportunistic yeast that is the most prevalent human fungal pathogen. While hypoxia is the predominant condition that C. albicans encounters in most of its niches, its impact on fungal metabolism remains unexplored so far. Here, we provided a detailed landscape of the C. albicans metabolome that emphasized the importance of many metabolic routes for the adaptation of this yeast to oxygen depletion. The fungal hypoxic metabolome identified in this work provides a framework for future investigations to assess the contribution of relevant metabolic pathways in the fitness of C. albicans and other human eukaryotic pathogens with similar colonized human niches. As hypoxia is present at most of the fungal infection foci in the host, hypoxic metabolic pathways are thus an attractive target for antifungal therapy.

scholarly journals Behavior of Yersinia enterocolitica in the Presence of the Bacterivorous Acanthamoeba castellanii

2013 ◽  
Vol 79 (20) ◽  
pp. 6407-6413 ◽  
Author(s):  
E. Lambrecht ◽  
J. Baré ◽  
I. Van Damme ◽  
W. Bert ◽  
K. Sabbe ◽  
...  
Keyword(s):  
Yersinia Enterocolitica ◽  
Pathogenic Bacteria ◽  
Acanthamoeba Castellanii ◽  
Ecological Niches ◽  
Free Living ◽  
Content Type ◽  
Food Borne ◽  
Transmission Electron ◽  
Set Up ◽  
The Impact

ABSTRACTFree-living protozoa play an important role in the ecology and epidemiology of human-pathogenic bacteria. In the present study, the interaction betweenYersinia enterocolitica, an important food-borne pathogen, and the free-living amoebaAcanthamoeba castellaniiwas studied. Several cocultivation assays were set up to assess the resistance ofY. enterocoliticatoA. castellaniipredation and the impact of environmental factors and bacterial strain-specific characteristics. Results showed that allY. enterocoliticastrains persist in association withA. castellaniifor at least 14 days, and associations withA. castellaniienhanced survival ofYersiniaunder nutrient-rich conditions at 25°C and under nutrient-poor conditions at 37°C. Amoebae cultivated in the supernatant of oneYersiniastrain showed temperature- and time-dependent permeabilization. Intraprotozoan survival ofY. enterocoliticadepended on nutrient availability and temperature, with up to 2.8 log CFU/ml bacteria displaying intracellular survival at 7°C for at least 4 days in nutrient-rich medium. Transmission electron microscopy was performed to locate theYersiniacells inside the amoebae. AsYersiniaandAcanthamoebashare similar ecological niches, this interaction identifies a role of free-living protozoa in the ecology and epidemiology ofY. enterocolitica.

scholarly journals A Comprehensive Coexpression Network Analysis in Vibrio cholerae

mSystems ◽  
2020 ◽  
Vol 5 (4) ◽  
Author(s):  
Cory D. DuPai ◽  
Claus O. Wilke ◽  
Bryan W. Davies
Keyword(s):  
Network Analysis ◽  
Vibrio Cholerae ◽  
Rna Sequencing ◽  
High Throughput Sequencing ◽  
Model Organism ◽  
Coexpression Network ◽  
Sequencing Data ◽  
Content Type ◽  
The Impact ◽  
Coexpression Network Analysis

ABSTRACT Research into the evolution and pathogenesis of Vibrio cholerae has benefited greatly from the generation of high-throughput sequencing data to drive molecular analyses. The steady accumulation of these data sets now provides a unique opportunity for in silico hypothesis generation via coexpression analysis. Here, we leverage all published V. cholerae RNA sequencing data, in combination with select data from other platforms, to generate a gene coexpression network that validates known gene interactions and identifies novel genetic partners across the entire V. cholerae genome. This network provides direct insights into genes influencing pathogenicity, metabolism, and transcriptional regulation, further clarifies results from previous sequencing experiments in V. cholerae (e.g., transposon insertion sequencing [Tn-seq] and chromatin immunoprecipitation sequencing [ChIP-seq]), and expands upon microarray-based findings in related Gram-negative bacteria. IMPORTANCE Cholera is a devastating illness that kills tens of thousands of people annually. Vibrio cholerae, the causative agent of cholera, is an important model organism to investigate both bacterial pathogenesis and the impact of horizontal gene transfer on the emergence and dissemination of new virulent strains. Despite the importance of this pathogen, roughly one-third of V. cholerae genes are functionally unannotated, leaving large gaps in our understanding of this microbe. Through coexpression network analysis of existing RNA sequencing data, this work develops an approach to uncover novel gene-gene relationships and contextualize genes with no known function, which will advance our understanding of V. cholerae virulence and evolution.

scholarly journals The Two-Component Signal Transduction System VxrAB Positively Regulates Vibrio cholerae Biofilm Formation

2017 ◽  
Vol 199 (18) ◽  
Author(s):  
Jennifer K. Teschler ◽  
Andrew T. Cheng ◽  
Fitnat H. Yildiz
Keyword(s):  
Signal Transduction ◽  
Vibrio Cholerae ◽  
Histidine Kinase ◽  
Biofilm Formation ◽  
Pathogenic Bacteria ◽  
Response Regulator ◽  
Systematic Analysis ◽  
Content Type ◽  
Two Component ◽  
Two Component Signal Transduction

ABSTRACT Two-component signal transduction systems (TCSs), typically composed of a sensor histidine kinase (HK) and a response regulator (RR), are the primary mechanism by which pathogenic bacteria sense and respond to extracellular signals. The pathogenic bacterium Vibrio cholerae is no exception and harbors 52 RR genes. Using in-frame deletion mutants of each RR gene, we performed a systematic analysis of their role in V. cholerae biofilm formation. We determined that 7 RRs impacted the expression of an essential biofilm gene and found that the recently characterized RR, VxrB, regulates the expression of key structural and regulatory biofilm genes in V. cholerae. vxrB is part of a 5-gene operon, which contains the cognate HK vxrA and three genes of unknown function. Strains carrying ΔvxrA and ΔvxrB mutations are deficient in biofilm formation, while the ΔvxrC mutation enhances biofilm formation. The overexpression of VxrB led to a decrease in motility. We also observed a small but reproducible effect of the absence of VxrB on the levels of cyclic di-GMP (c-di-GMP). Our work reveals a new function for the Vxr TCS as a regulator of biofilm formation and suggests that this regulation may act through key biofilm regulators and the modulation of cellular c-di-GMP levels. IMPORTANCE Biofilms play an important role in the Vibrio cholerae life cycle, providing protection from environmental stresses and contributing to the transmission of V. cholerae to the human host. V. cholerae can utilize two-component systems (TCS), composed of a histidine kinase (HK) and a response regulator (RR), to regulate biofilm formation in response to external cues. We performed a systematic analysis of V. cholerae RRs and identified a new regulator of biofilm formation, VxrB. We demonstrated that the VxrAB TCS is essential for robust biofilm formation and that this system may regulate biofilm formation via its regulation of key biofilm regulators and cyclic di-GMP levels. This research furthers our understanding of the role that TCSs play in the regulation of V. cholerae biofilm formation.

scholarly journals Contribution of Asparagine Catabolism to Salmonella Virulence

2016 ◽  
Vol 85 (2) ◽  
Author(s):  
Patrick A. McLaughlin ◽  
Michael McClelland ◽  
Hee-Jeong Yang ◽  
Steffen Porwollik ◽  
Lydia Bogomolnaya ◽  
...  
Keyword(s):  
T Cell ◽  
Pathogenic Bacteria ◽  
Protein A ◽  
Metabolic Reprogramming ◽  
Wild Type ◽  
Content Type ◽  
Cell Responses ◽  
Serovar Typhimurium ◽  
Salmonella Virulence ◽  
And Function

ABSTRACT Salmonellae are pathogenic bacteria that cause significant morbidity and mortality in humans worldwide. Salmonellae establish infection and avoid clearance by the immune system by mechanisms that are not well understood. We previously showed that l-asparaginase II produced by Salmonella enterica serovar Typhimurium (S. Typhimurium) inhibits T cell responses and mediates virulence. In addition, we previously showed that asparagine deprivation such as that mediated by l-asparaginase II of S. Typhimurium causes suppression of activation-induced T cell metabolic reprogramming. Here, we report that STM3997, which encodes a homolog of disulfide bond protein A (dsbA) of Escherichia coli, is required for l-asparaginase II stability and function. Furthermore, we report that l-asparaginase II localizes primarily to the periplasm and acts together with l-asparaginase I to provide S. Typhimurium the ability to catabolize asparagine and assimilate nitrogen. Importantly, we determined that, in a murine model of infection, S. Typhimurium lacking both l-asparaginase I and II genes competes poorly with wild-type S. Typhimurium for colonization of target tissues. Collectively, these results indicate that asparagine catabolism contributes to S. Typhimurium virulence, providing new insights into the competition for nutrients at the host-pathogen interface.

Central role of the Na+-translocating NADH:quinone oxidoreductase (Na+-NQR) in sodium bioenergetics of Vibrio cholerae

2014 ◽  
Vol 395 (12) ◽  
pp. 1389-1399 ◽  
Author(s):  
Julia Steuber ◽  
Petra Halang ◽  
Thomas Vorburger ◽  
Wojtek Steffen ◽  
Georg Vohl ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Cytoplasmic Membrane ◽  
Sea Water ◽  
Three Dimensional ◽  
Transport Processes ◽  
Dimensional Structure ◽  
Substrate Uptake ◽  
Molecular Architecture ◽  
Nadh:Quinone Oxidoreductase

Abstract Vibrio cholerae is a Gram-negative bacterium that lives in brackish or sea water environments. Strains of V. cholerae carrying the pathogenicity islands infect the human gut and cause the fatal disease cholera. Vibrio cholerae maintains a Na+ gradient at its cytoplasmic membrane that drives substrate uptake, motility, and efflux of antibiotics. Here, we summarize the major Na+-dependent transport processes and describe the central role of the Na+-translocating NADH:quinone oxidoreductase (Na+-NQR), a primary Na+ pump, in maintaining a Na+-motive force. The Na+-NQR is a membrane protein complex with a mass of about 220 kDa that couples the exergonic oxidation of NADH to the transport of Na+ across the cytoplasmic membrane. We describe the molecular architecture of this respiratory complex and summarize the findings how electron transport might be coupled to Na+-translocation. Moreover, recent advances in the determination of the three-dimensional structure of this complex are reported.

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