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M K Jain

Publications and source records attributed to M K Jain.

At least 37 records · Page 2Linked to original sources
PubMed2000

Structural basis of the anionic interface preference and kcat* activation of pancreatic phospholipase A2.

Pancreatic phospholipase A(2) (PLA2) shows a strong preference for the binding to the anionic interface and a consequent allosteric activation. In this paper, we show that virtually all the preference is mediated through 3 (Lys-53, -56, and -120) of the 12 cationic residues of bovine pancreatic PLA2. The lysine-to-methionine substitution enhances the binding of the enzyme to the zwitterionic interface, and for the K53,56,120M triple mutant at the zwitterionic interface is comparable to that for the wild type (WT) at the anionic interface. In the isomorphous crystal structure, the backbone folding of K53,56M K120,121A and WT are virtually identical, yet a significant change in the side chains of certain residues, away from the site of substitution, mostly at the putative contact site with the interface (i-face), is discernible. Such reciprocity, also supported by the spectroscopic results for the free and bound forms of the enzyme, is expected because a distal structural change that perturbs the interfacial binding could also affect the i-face. The results show that lysine-to-methionine substitution induces a structural change that promotes the binding of PLA2 to the interface as well as the substrate binding to the enzyme at the interface. The kinetic results are consistent with a model in which the interfacial Michaelis complex exists in two forms, and the complex that undergoes the chemical step is formed by the charge compensation of Lys-53 and -56. Analysis of the incremental changes in the kinetic parameters shows that the charge compensation of Lys-53 and -56 contributes to the activation and that of Lys-120 contributes only to the structural change that promotes the stability of the Michaelis complex at the interface. The charge compensation effects on these three residues also account for the differences in the anionic interface preference of the evolutionarily divergent secreted PLA2.

Amino Acid Substitution↗
PubMed2000

1-Cys peroxiredoxin, a bifunctional enzyme with glutathione peroxidase and phospholipase A2 activities.

This report provides definitive evidence that the protein 1-Cys peroxiredoxin is a bifunctional ("moonlighting") enzyme with two distinct active sites. We have previously shown that human, rat, and bovine lungs contain an acidic Ca(2+)-independent phospholipase A(2) (aiPLA(2)). The cDNA encoding aiPLA(2) was found to be identical to that of a non-selenium glutathione peroxidase (NSGPx). Protein expressed using a previously reported E. coli construct which has a His-tag and 50 additional amino acids at the NH(2) terminus, did not exhibit aiPLA(2) activity. A new construct which contains the His-tag plus two extra amino acids at the COOH terminus when expressed in Escherichia coli generated a protein that hydrolyzed the sn-2 acyl chain of phospholipids at pH 4, and exhibited NSGPx activity with H(2)O(2) at pH 8. The expressed 1-Cys peroxiredoxin has identical functional properties to the native lung enzyme: aiPLA(2) activity is inhibited by the serine protease inhibitor, diethyl p-nitrophenyl phosphate, by the tetrahedral mimic 1-hexadecyl-3-trifluoroethylglycero-sn-2-phosphomethanol (MJ33), and by 1-Cys peroxiredoxin monoclonal antibody (mAb) 8H11 but these agents have no effect on NSGPx activity; NSGPx activity is inhibited by mercaptosuccinate and by 1-Cys peroxiredoxin mAb 8B3 antibody which have no effect on aiPLA(2) activity. Mutation of Ser(32) to Ala abolishes aiPLA(2) activity, yet the NSGPx activity remains unaffected; a Cys(47) to Ser mutant is devoid of peroxidase activity but aiPLA(2) activity remains intact. These results suggest that Ser(32) in the GDSWG consensus sequence provides the catalytic nucleophile for the hydrolase activity of aiPLA(2), while Cys(47) in the PVCTTE consensus sequence is at the active site for peroxidase activity. The bifunctional catalytic properties of 1-Cys peroxiredoxin are compatible with a simultaneous role for the protein in the regulation of phospholipid turnover as well as in protection against oxidative injury.

Antioxidants↗
PubMed2000

Transforming growth factor-beta 1 inhibits cytokine-mediated induction of human metalloelastase in macrophages.

Matrix metalloproteinases (MMP) have been identified in vulnerable areas of atherosclerotic plaques and may contribute to plaque instability through extracellular matrix degradation. Human metalloelastase (MMP-12) is a macrophage-specific MMP with broad substrate specificity and is capable of degrading proteins found in the extracellular matrix of atheromas. Despite its potential importance, little is known about the regulation of MMP-12 expression in the context of atherosclerosis. In this study, we report that in human peripheral blood-derived macrophages, MMP-12 mRNA was markedly up-regulated by several pro-atherosclerotic cytokines and growth factors including interleukin-1beta, tumor necrosis factor-alpha, macrophage colony-stimulating factor, vascular endothelial growth factor, and platelet-derived growth factor-BB. In contrast, the pleiotropic anti-inflammatory growth factor transforming growth factor-beta1 (TGF-beta1) inhibited cytokine-mediated induction of MMP-12 mRNA, protein, and enzymatic activity. Analyses of MMP-12 promoter through transient transfections and electrophoretic mobility shift assays indicated that both its induction by cytokines and its inhibition by TGF-beta1 depended on signaling through an AP-1 site at -81 base pairs. Moreover, the inhibitory effect of TGF-beta1 on MMP-12 was dependent on Smad3. Taken together, MMP-12 is induced by several factors implicated in atherosclerosis. The inhibition of MMP-12 expression by TGF-beta1 suggests that TGF-beta1, acting via Smad3, may promote plaque stability.

Animals↗
PubMed2000

Control of the chemical step by leucine-31 of pancreatic phospholipase A2.

A well-defined region of pancreatic and other secreted phospholipase A2 (PLA2), which we call the i-face, makes a molecular contact with the interface to facilitate and control the events and processivity of the interfacial catalytic turnover cycles. The structural features of the i-face and its allosteric relationship to the active site remain to be identified. As a part of the calcium binding (26-34) loop, Leu-31 is located on the surface near the substrate binding slot of PLA2. Analysis of the primary rate and equilibrium parameters of the Leu-31 substitution mutants of the pig pancreatic PLA2 shows that the only significant effect of the substitution is to impair the chemical step at the zwitterionic interface in the presence of added NaCl, and only a modest effect is seen on kcat at the anionic interface. Leu-31 substitutions have little effect on the binding of the enzyme to the interface; the affinity for certain substrate mimics is modestly influenced in W3F, L31W double mutant. The fluorescence emission results with the double mutant show that the microenvironment of Trp-31 is qualitatively different at the zwitterionic versus anionic interfaces. At both of the interfaces Trp-31 is not shielded from the bulk aqueous environment as it remains readily accessible to acrylamide and water. The NaCl-induced change in the Trp-31 emission spectrum of the double mutant on the zwitterionic interface is similar to that seen on the binding to the anionic interface. Together, the kinetic and spectroscopic results show that the form of PLA2 at the zwitterionic interface (Ez) is distinguishably different from the catalytically more efficient form at the anionic interface (Ea). This finding provides a structural basis for the two-state model for kcat activation by the anionic interface. In conjunction with earlier results we suggest that neutralization of certain cationic residues of PLA2 exerts a control on the calcium loop through residue 31.

Amino Acid Substitution↗
PubMed2000

Cardiovascular basic helix loop helix factor 1, a novel transcriptional repressor expressed preferentially in the developing and adult cardiovascular system.

We have cloned a cardiovascular-restricted basic helix-loop-helix factor that interacts with arylhydrocarbon receptor nuclear translocator (ARNT) in a yeast two-hybrid screen. Cardiovascular helix-loop-helix factor 1 (CHF1) is distantly related to the hairy family of transcriptional repressors. We analyzed its expression pattern during mouse embryo development. At day 8.5, the expression of CHF1 is first detected in the primitive ventricle of the primordial heart tube and persists throughout gestation. In rat hearts, this expression is down-regulated after birth, concurrent with terminal differentiation of cardiomyocytes. In the developing vasculature, CHF1 first appears in the dorsal aorta at day 9.0, which precedes the reported expression of smooth muscle cell markers, and persists into adulthood. In an in vitro system of smooth muscle cell differentiation, CHF1 mRNA was barely detectable in undifferentiated cells but was induced highly in differentiated smooth muscle cells. To determine whether CHF1 might affect the function of ARNT, we performed transfection studies. Co-transfection of CHF1 inhibited ARNT/EPAS1-dependent transcription by 85%, and this inhibition is dose-dependent. In electrophoretic mobility studies, CHF1 inhibited the binding of the ARNT/EPAS1 heterodimer to its target site. Our data suggest that CHF1 functions as a transcriptional repressor and may play an important role in cardiovascular development.

Animals↗
PubMed2000

Cationic peptide antimicrobials induce selective transcription of micF and osmY in Escherichia coli.

Cationic antimicrobial peptides, such as polymyxin and cecropin, activated transcription of osmY and micF in growing Escherichia coli independently of each other. The micF response required the presence of a functional rob gene. It is intriguing that in this and other assays an identical response profile was also seen with hyperosmotic salt or sucrose gradient, two of the most commonly used traditional food preservatives. The osmY and micF transcription was not induced by hypoosmotic gradient, ionophoric peptides, uncouplers, or with other classes of membrane perturbing agents. The antibacterial peptides did not promote transcription of genes that respond to macromolecular or oxidative damage, fatty acid biosynthesis, heat shock, or depletion of proton or ion gradients. These and other results show that the antibacterial cationic peptides induce stasis in the early growth phase, and the transcriptional efficacy of antibacterial peptides correlates with their minimum inhibitory concentration, and also with their ability to mediate direct exchange of phospholipids between vesicles. The significance of these results is developed as the hypothesis that the cationic peptide antimicrobials stress growth of Gram-negative organisms by making contacts between the two phospholipid interfaces in the periplasmic space and prevent the hyperosmotic wrinkling of the cytoplasmic membrane. Broader significance of these results, and of the hypothesis that the peptide mediated contacts between the periplasmic phospholipid interfaces are the primary triggers, is discussed in relation to antibacterial resistance.

Adaptation, Physiological↗
PubMed2000

Origin of antibacterial stasis by polymyxin B in Escherichia coli.

We show that blockage of hyperosmotic shock induced plasmolysis by polymyxin B (PxB) is related to its selective antimicrobial action against Gram-negative organisms. The rapid wrinkling of the cytoplasmic membrane induced by the hyperosmotic shrinkage of cytoplasmic volume due to the water efflux is monitored as an increase in the 90 degrees light scattering. The rapid scattering response is complete within 1 min after the addition of hyperosmolar NaCl. PxB decreases the amplitude of the rapid increase in the light scattering due to the shrinkage of the cytoplasmic volume by hyperosmotic shock. The amplitude is highest with cells in the early log phase of growth. The effect of PxB is induced rapidly and the maximum effect is seen within 1 min preincubation of cells. The effect of PxB is concentration dependent, and about 50% decrease in the amplitude is seen in the range of the growth inhibitory concentrations of PxB. The effect of PxB is not seen if added after the onset of the up-shock. As a heuristic model we suggest that PxB forms contacts between the two phospholipid interfaces that enclose the periplasmic space. The plasmolytic response results with osmY(-) mutant suggest that, like PxB, the osmY gene product in the periplasmic space prevents the shrinkage of the cytoplasmic compartment. Since PxB induces osmY transcription, we propose that, as a possible locus for the origin of the PxB induced stress, a contact between the phospholipid interfaces surrounding the periplasmic space triggers the metabolic changes leading to bacterial stasis.

Anti-Bacterial Agents↗
PubMed2000

In vitro temperature map of cardiac ablation demonstrates the effect of flow on lesion development.

This paper presents an in vitro temperature mapping study of bovine cardiac tissue during radiofrequency ablation. The objectives were to: (i) develop a technique for measuring the spatial and temporal temperature distribution in the tissue and in the blood during ablation, and (ii) use the temperature measurements to characterize the effects of fluid flow on lesion dimensions, ablation efficiency, and temperature distributions. In vitro ablation (20 W, 60 s) of bovine cardiac tissue was performed. The tissue was placed in a saline-dextrose solution maintained at 37+/- 0.5 degrees C. The solution also irrigated the tissue surface and simulated blood flow velocities of (i) 30, (ii) 55, and (iii) 85 mm/s. Thermocouple measurements were recorded from 25 and 2 locations in the tissue and in the fluid, respectively. The lowest flow resulted in the largest lesion, the maximum tissue, fluid, and electrode temperature increases, and the highest ablation efficiency. The lesions were 5.8 +/- 0.81, 4.8 +/- 0.84, and 4.4 +/- 1.25 mm deep, and 9.3 +/- 1.07, 7.9 +/- 1.48, and 7.8 +/- 1.27 mm wide for flows (i)-(iii), respectively. The blood and tissue temperature distributions were asymmetric around the ablating electrode axis with higher temperatures on the outflow than on the inflow side. The experimental measurements were used to validate a numeric model of ablation in an accompanying paper.

Animals↗
PubMed2000

A three-dimensional finite element model of radiofrequency ablation with blood flow and its experimental validation.

A novel three-dimensional finite element model for the study of radiofrequency ablation is presented. The model was used to perform an analysis of the temperature distribution in a tissue block heated by RF energy and cooled by blood (fluid) flow. This work extends earlier models by including true flow in place of a convective boundary condition to simulate realistic experimental conditions and to improve the prediction of blood temperatures. The effect of fluid flow on the temperature distribution, the lesion dimensions, and the ablation efficiency was studied. Three flow velocities were simulated: (i) 30, (ii) 55, and (iii) 85 mm/s. The modeling results were validated qualitatively and quantitatively with in vitro data. The correlation coefficients between the modeling and the experimental temperature measurements were 0.98, 0.97, and 0.95 for flows (i)-(iii), respectively. The slopes were 0.89, 0.95, and 1.06, and the mean root mean square differences between modeling and experimental temperature measurements were 17.3% +/- 11.6%, 15.8% +/- 13.4%, and 18.8% +/- 14.9% for flows (i)-(iii), respectively. A comparison of temperature distribution obtained with a convective boundary versus inclusion of fluid motion showed that the convective boundary resulted in a similar tissue temperature distribution, but overestimated fluid temperatures and lacked the flow asymmetry seen in the true flow model.

Arrhythmias, Cardiac↗
PubMed1999

Generation of a dominant-negative mutant of endothelial PAS domain protein 1 by deletion of a potent C-terminal transactivation domain.

Endothelial PAS domain protein 1 (EPAS1) is a basic helix-loop-helix/PAS domain transcription factor that is preferentially expressed in vascular endothelial cells. EPAS1 shares high homology with hypoxia-inducible factor-1alpha (HIF-1alpha) and, like HIF-1alpha, has been shown to bind to the HIF-1-binding site and to activate its downstream genes such as vascular endothelial growth factor (VEGF) and erythropoietin. In this report, we show that EPAS1 increased VEGF gene expression through the HIF-1-binding site. This transactivation was enhanced further by cotransfection of an aryl hydrocarbon receptor nuclear translocator expression plasmid. Deletion analysis of EPAS1 revealed a potent activation domain (amino acids 486-639) essential for EPAS1 to transactivate the VEGF promoter. We confirmed the ability of this domain to activate transcription using a Gal4 fusion protein system. Because a truncated EPAS1 protein lacking the transactivation domain at amino acids 486-639 eliminated induction of the VEGF promoter by wild-type EPAS1, the truncated protein functions as a dominant-negative mutant. Most important, infection of the cells with an adenoviral construct expressing this mutant inhibited the induction of VEGF mRNA under conditions that mimic hypoxia. Our results suggest that EPAS1 is an important regulator of VEGF gene expression. Since VEGF plays a crucial role in angiogenesis, the ability of dominant-negative EPAS1 to inhibit VEGF promoter activity raises the possibility of a novel approach to inhibiting pathological angiogenesis.

Animals↗
PubMed1999

Membrane-bound plasma platelet activating factor acetylhydrolase acts on substrate in the aqueous phase.

Human plasma platelet activating factor acetylhydrolase (pPAF-AH) is a phospholipase A(2) that specifically hydrolyzes the sn-2 ester of platelet activating factor (PAF) and of phospholipids with oxidatively truncated sn-2 fatty acyl chains. pPAF-AH is bound to lipoproteins in vivo, and it binds essentially irreversibly to anionic and zwitterionic phospholipid vesicles in vitro and hydrolyzes PAF and PAF analogues. Substrate hydrolysis also occurs in the absence of vesicles, with a maximum rate reached at the critical micelle concentration. A novel pre-steady-state kinetic analysis with enzyme tightly bound to vesicles and with a substrate that undergoes slow intervesicle exchange establishes that pPAF-AH accesses its substrate from the aqueous phase and thus is not an interfacial enzyme. Such a mechanism readily explains why this enzyme displays dramatic specificity for phospholipids with short sn-2 chains or with medium-length, oxidatively truncated sn-2 chains since a common feature of these lipids is their relatively high water solubility. It also explains why the enzymatic rate drops as the length of the sn-1 chain is increased. pPAF-AH shows broad specificity toward phospholipids with different polar headgroups. Additional results are that PAF undergoes intervesicle exchange on the subminute time scale and it does not undergo transbilayer movement over tens of minutes.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1999

Hydrolysis of monodisperse phosphatidylcholines by phospholipase A2 occurs on vessel walls and air bubbles.

Hydrolysis of monodisperse short chain phosphatidylcholines, far below their critical micelle concentration, by phospholipase A2 (PLA2) and other interfacial enzymes is characterized. Results show that virtually all the observed hydrolysis by pancreatic and human inflammatory PLA2 occurs on surfaces of the reaction vessel or air bubbles. Conditions to eliminate such extraneous contributions at low substrate concentrations are established. Premicellar aggregates are apparently formed near the critical micelle concentration. The observation window at low substrate concentrations is used to obtain an upper limit estimate of the rate of hydrolysis through the monodisperse Michaelis complex. A limit estimate of <0.1 s-1 is obtained for the hydrolysis of monodisperse substrates by pig pancreatic phospholipase A2. These results show that the observed rate of hydrolysis of dihexanoyl- and diheptanoylphosphatidylcholines with pig pancreatic phospholipase A(2) through the monomer path is insignificant compared to the rate of >1000 s-1 seen at the saturating levels of the micellar substrate. These protocols should be useful for evaluating reactions catalyzed at vessel walls. Implications of these results for assays and models of interfacial activation of pancreatic PLA2 are discussed.

Adsorption↗
PubMed1999

Contributions of residues of pancreatic phospholipase A2 to interfacial binding, catalysis, and activation.

Primary rate and equilibrium parameters for 60 site-directed mutants of bovine pancreatic phospholipase A2 (PLA2) are analyzed so incremental contributions of the substitution of specific residues can be evaluated. The magnitude of the change is evaluated so a functional role in the context of the N- and C-domains of PLA2 can be assigned, and their relationship to the catalytic residues and to the i-face that makes contact with the interface. The effect of substitutions and interfacial charge is characterized by the equilibrium dissociation constant for dissociation of the bound enzyme from the interface (Kd), the dissociation constant for dissociation of a substrate mimic from the active site of the bound enzyme (KL), and the interfacial Michaelis constants, KM and kcat. Activity is lost (>99.9%) on the substitution of H48 and D49, the catalytic residues. A more than 95% decrease in kcat is seen with the substitution of F5, I9, D99, A102, or F106, which form the substrate binding pocket. Certain residues, which are not part of the catalytic site or the substrate binding pocket, also modulate kcat. Interfacial anionic charge lowers Kd, and induces kcat activation through K56, K53, K119, or K120. Significant changes in KL are seen by the substitution of N6, I9, F22, Y52, K53, N71, Y73, A102, or A103. Changes in KM [=(k2+k-1)/k1] are attributed to kcat (=k2) and KL (=k-1/k1). Some substitutions change more than one parameter, implying an allosteric effect of the binding to the interface on KS, and the effect of the interfacial anionic charge on kcat. Interpreted in the context of the overall structure, results provide insights into the role of segments and domains in the microscopic events of catalytic turnover and processivity, and their allosteric regulation. We suggest that the interfacial recognition region (i-face) of PLA2, due to the plasticity of certain segments and domains, exercises an allosteric control on the substrate binding and chemical step.

Animals↗
PubMed1999

Induction of high mobility group I architectural transcription factors in proliferating vascular smooth muscle in vivo and in vitro.

Proliferation of vascular smooth muscle cells (VSMCs) is a hallmark of arteriosclerosis. Architectural transcription factors of the high mobility group (HMG)-I family have been implicated in the control of cell proliferation and gene expression. We studied the pattern of HMG-I mRNA and protein expression in proliferating VSMCs. HMG-I(Y) and HMGI-C mRNAs were barely detectable by Northern analysis in samples prepared from uninjured rat carotid arteries. In contrast, these mRNAs were induced dramatically in carotid arteries 2 and 5-6 days after balloon injury. By in situ hybridization at 6 days after injury, the induced mRNAs localized to smooth muscle cells of the developing neointima, and immunocytochemical analysis showed that HMG-I(Y) protein was expressed in the nuclei of these cells. To confirm this association between HMG-I protein induction and cell growth, we assessed HMG-I(Y) and HMGI-C mRNA expression in rat aortic smooth muscle cells (RASMCs) in primary culture. The HMG-I mRNAs were barely detectable in quiescent RASMCs but were induced markedly by serum stimulation. This induction of mRNA by serum was time dependent and peaked at 9 h. Western blot analysis confirmed that HMG-I(Y) protein induction also occurred in vitro. To our knowledge, this is the first demonstration of induction of HMG-I protein expression in proliferating RASMCs in vivo and in vitro. This demonstration suggests that the HMG-I proteins may play an important role in smooth muscle cell proliferation.

Animals↗
PubMed1999

Actinobacillus succinogenes sp. nov., a novel succinic-acid-producing strain from the bovine rumen.

Strain 130ZT was isolated from the bovine rumen. It is a facultatively anaerobic, pleomorphic, Gram-negative rod. It exhibits a 'Morse code' form of morphology, which is characteristic of the genus Actinobacillus. Strain 130ZT is a capnophilic, osmotolerant succinogen that utilizes a broad range of sugars. It accumulates high concentrations of succinic acid (> 70 g l-1). Strain 130ZT is positive for catalase, oxidase, alkaline phosphatase and beta-galactosidase, but does not produce indole or urease. Acid but no gas is produced from D-glucose and D-fructose. 16S rRNA sequence analysis places strain 130ZT within the family Pasteurellaceae; the most closely related members of the family Pasteurellaceae have 16S rRNA similarities of 95.5% or less with strain 130ZT. Strain 130ZT was compared with Actinobacillus lignieresii and the related Bisgaard Taxa 6 and 10. Based upon morphological and biochemical properties, strain 130ZT is most similar to members of the genus Actinobacillus within the family Pasteurellaceae. It is proposed that strain 130ZT be classified as a new species, Actinobacillus succinogenes. The type strain of Actinobacillus succinogenes sp. nov. is ATCC 55618T.

Actinobacillus↗
PubMed1999

Temperature-controlled and constant-power radio-frequency ablation: what affects lesion growth?

Radio-frequency (RF) catheter ablation is the primary interventional therapy for the treatment of many cardiac tachyarrhythmias. Three-dimensional finite element analysis of constant-power (CPRFA) and temperature-controlled RF ablation (TCRFA) of the endocardium is performed. The objectives are to study: 1) the lesion growth with time and 2) the effect of ground electrode location on lesion dimensions and ablation efficiency. The results indicate that: a) for TCRFA: i) lesion growth was fastest during the first 20 s, subsequently the lesion growth slowed reaching a steady state after 100 s, ii) positioning the ground electrode directly opposite the catheter tip (optimal) produced a larger lesion, and iii) a constant tip temperature maintained a constant maximum tissue temperature; b) for CPRFA: i) the lesion growth was fastest during the first 20 s and then the lesion growth slowed; however, the lesion size did not reach steady state even after 600 s suggesting that longer durations of energy delivery may result in wider and deeper lesions, ii) the temperature-dependent electrical conductivity of the tissue is responsible for this continuous lesion growth, and iii) an optimal ground electrode location resulted in a slightly larger lesion and higher ablation efficiency.

Arrhythmias, Cardiac↗
PubMed1999

Microbial utilization of electrically reduced neutral red as the sole electron donor for growth and metabolite production.

Electrically reduced neutral red (NR) served as the sole source of reducing power for growth and metabolism of pure and mixed cultures of H2-consuming bacteria in a novel electrochemical bioreactor system. NR was continuously reduced by the cathodic potential (-1.5 V) generated from an electric current (0.3 to 1.0 mA), and it was subsequently oxidized by Actinobacillus succinogenes or by mixed methanogenic cultures. The A. succinogenes mutant strain FZ-6 did not grow on fumarate alone unless electrically reduced NR or hydrogen was present as the electron donor for succinate production. The mutant strain, unlike the wild type, lacked pyruvate formate lyase and formate dehydrogenase. Electrically reduced NR also replaced hydrogen as the sole electron donor source for growth and production of methane from CO2. These results show that both pure and mixed cultures can function as electrochemical devices when electrically generated reducing power can be used to drive metabolism. The potential utility of utilizing electrical reducing power in enhancing industrial fermentations or biotransformation processes is discussed.

Actinobacillus↗