In general terms, this thesis is about tuning coupled electronic and nuclear (or mechanical) dynamics in the nanoscale. With “tuning” we mean changing parameters to achieve a specific phenomenon or functionality. This is not a trivial task in this context, because the dynamics of the systems we consider depend nontrivially on the parameters. To be more concrete, we consider two systems which are “complimentary” in many aspects. We start by studying nonradiative decay of an electronic excitation in a minimal example from supramolecular chemistry: a molecular dimer. Each monomer in our model has two electronic states and the respective potential energy surfaces (PESs) are harmonic. Electronic de-excitation occurs in the monomeric level through well-localized regions in the nuclear space which we call ``NRD channels\'\'. The monomers interact via transition dipole-dipole interaction. The decay dynamics of the monomer are trivial due to its harmonic PESs and simple NRD channel. However, the dimer shows distorted and nontrivially coupled PESs conferring rather complex decay dynamics on it. Depending on the position of the NRD channel, we find that the NRD lifetime can exhibit a completely different dependence on the intermolecular-interaction strength. The extension to larger aggregates and the implications to the quantum yield of molecular systems will be discussed. Our findings suggest design principles for molecular systems where a specific fluorescence quantum yield is desired. The most part of this thesis is about a nanoscale rotor driven by charge tunneling. The rotor consists of electronic islands linked to a bearing via insulating arms. The islands can exchange electrons via tunneling with flanking electronic leads. An uniform electrostatic field brings about the coupling between electronic and mechanical degrees of freedom. Moreover, coupling to an environment lead to dissipation in the mechanical dynamics. In the literature one can identify two generic models of this type of rotor [1-3], which we refer to as “mean-field” and “stochastic” models in this thesis. In the mean-field model the system is described by a set of deterministic differential equations involving the average charge on the electronic islands, and therefore charge fluctuations are not taken into account. In the stochastic model the rotor is described by Fokker–Planck equations which fully take into account the charge fluctuations. We start by showing and comparing the dynamics of these models. The models show interesting phenomenology and predict useful functionality to the rotor. However, it is often unclear which assumptions are made upon the system when using these models. To clarify this matter we derived the models using the “orthodox” theory of single electron tunneling [4]. Next, we go on and propose experimental devices which can be described by these models. The parameter ranges accessible using these devices are estimated. Turning our attention back to functionality, we show how to introduce a preferred direction of rotation, which is useful in the context of motors. In the outlook we also show how to recast the system as a current rectifier. [1] A. Y. Smirnov, S. Savel’ev, L. G. Mourokh and F. Nori; Phys. Rev. E 78 031921 (2008). [2] A. Croy and A. Eisfeld; EPL (Europhysics Lett. 98 68004 (2012). [3] A. Smirnov, L. Murokh, S. Savel’ev and F. Nori; Bio-mimicking rotary nanomotors; volume 7364 (2009); doi:10.1117/12.821567; URL http://dx.doi.org/10.1117/12. 821567. [4] B. L. Altshuler, P. A. Lee and W. R. Webb; Mesoscopic phenomena in solids; volume 30; Elsevier (2012).

In general terms, this thesis is about tuning coupled electronic and nuclear (or mechanical) dynamics in the nanoscale. With “tuning” we mean changing parameters to achieve a specific phenomenon or functionality. This is not a trivial task in this context, because the dynamics of the systems we consider depend nontrivially on the parameters. To be more concrete, we consider two systems which are “complimentary” in many aspects. We start by studying nonradiative decay of an electronic excitation in a minimal example from supramolecular chemistry: a molecular dimer. Each monomer in our model has two electronic states and the respective potential energy surfaces (PESs) are harmonic. Electronic de-excitation occurs in the monomeric level through well-localized regions in the nuclear space which we call ``NRD channels\'\'. The monomers interact via transition dipole-dipole interaction. The decay dynamics of the monomer are trivial due to its harmonic PESs and simple NRD channel. However, the dimer shows distorted and nontrivially coupled PESs conferring rather complex decay dynamics on it. Depending on the position of the NRD channel, we find that the NRD lifetime can exhibit a completely different dependence on the intermolecular-interaction strength. The extension to larger aggregates and the implications to the quantum yield of molecular systems will be discussed. Our findings suggest design principles for molecular systems where a specific fluorescence quantum yield is desired. The most part of this thesis is about a nanoscale rotor driven by charge tunneling. The rotor consists of electronic islands linked to a bearing via insulating arms. The islands can exchange electrons via tunneling with flanking electronic leads. An uniform electrostatic field brings about the coupling between electronic and mechanical degrees of freedom. Moreover, coupling to an environment lead to dissipation in the mechanical dynamics. In the literature one can identify two generic models of this type of rotor [1-3], which we refer to as “mean-field” and “stochastic” models in this thesis. In the mean-field model the system is described by a set of deterministic differential equations involving the average charge on the electronic islands, and therefore charge fluctuations are not taken into account. In the stochastic model the rotor is described by Fokker–Planck equations which fully take into account the charge fluctuations. We start by showing and comparing the dynamics of these models. The models show interesting phenomenology and predict useful functionality to the rotor. However, it is often unclear which assumptions are made upon the system when using these models. To clarify this matter we derived the models using the “orthodox” theory of single electron tunneling [4]. Next, we go on and propose experimental devices which can be described by these models. The parameter ranges accessible using these devices are estimated. Turning our attention back to functionality, we show how to introduce a preferred direction of rotation, which is useful in the context of motors. In the outlook we also show how to recast the system as a current rectifier. [1] A. Y. Smirnov, S. Savel’ev, L. G. Mourokh and F. Nori; Phys. Rev. E 78 031921 (2008). [2] A. Croy and A. Eisfeld; EPL (Europhysics Lett. 98 68004 (2012). [3] A. Smirnov, L. Murokh, S. Savel’ev and F. Nori; Bio-mimicking rotary nanomotors; volume 7364 (2009); doi:10.1117/12.821567; URL http://dx.doi.org/10.1117/12. 821567. [4] B. L. Altshuler, P. A. Lee and W. R. Webb; Mesoscopic phenomena in solids; volume 30; Elsevier (2012).

No description available.

The aim of this study was to determine if the dietary benefits of bioflavonoids are linked to the inhibition of ATP synthase. We studied the inhibitory effect of 17 bioflavonoid compounds on purified F1 or membrane bound F1Fo E. coli ATP synthase. We found that the extent of inhibition by bioflavonoid compounds was variable. Morin, silymarin, baicalein, silibinin, rimantadin, amantidin, or, epicatechin resulted in complete inhibition. The most potent inhibitors on molar scale were morin (IC50∼0.07mM)>silymarin (IC50∼0.11mM)>baicalein (IC50∼0.29mM)>silibinin (IC50∼0.34mM)>rimantadin (IC50∼2.0mM)>amantidin (IC50∼2.5mM)>epicatechin (IC50∼4.0mM). Inhibition by hesperidin, chrysin, kaempferol, diosmin, apigenin, genistein, or rutin was partial in the range of 40-60% and inhibition by galangin, daidzein, or luteolin was insignificant. The main skeleton, size, shape, geometry, and position of functional groups on inhibitors played important role in the effective inhibition of ATP synthase. In all cases inhibition was found fully reversible and identical in both F1Fo membrane preparations and isolated purified F1. ATPase and growth assays suggested that the bioflavonoid compounds used in this study inhibited F1-ATPase as well as ATP synthesis nearly equally, which signifies a link between the beneficial effects of dietary bioflavonoids and their inhibitory action on ATP synthase.

Self-propelled microjet engines (microbots) can transport multiple cells into specific locations in a fluid. The motion is externally controlled by a magnetic field which allows to selectively load, transport and deliver the cells. / Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.

Self-propelled microjet engines (microbots) can transport multiple cells into specific locations in a fluid. The motion is externally controlled by a magnetic field which allows to selectively load, transport and deliver the cells. / Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.

We have studied the inhibitory effect of five polyphenols namely, resveratrol, piceatannol, quercetin, quercetrin, and quercetin-3-β-d glucoside on Escherichia coli ATP synthase. Recently published X-ray crystal structures of bovine mitochondrial ATP synthase inhibited by resveratrol, piceatannol, and quercetin, suggest that these compounds bind in a hydrophobic pocket between the γ-subunit C-terminal tip and the hydrophobic inside of the surrounding annulus in a region critical for rotation of the γ-subunit. Herein, we show that resveratrol, piceatannol, quercetin, quercetrin, or quercetin-3-β-d glucoside all inhibit E. coli ATP synthase but to different degrees. Whereas piceatannol inhibited ATPase essentially completely (∼0 residual activity), inhibition by other compounds was partial with ∼20% residual activity by quercetin, ∼50% residual activity by quercetin-3-β-d glucoside, and ∼60% residual activity by quercetrin or resveratrol. Piceatannol was the most potent inhibitor (IC50 ∼14 μM) followed by quercetin (IC50 ∼33 μM), quercetin-3-β-d glucoside (IC50 ∼71 μM), resveratrol (IC50 ∼94 μM), quercitrin (IC50 ∼120 μM). Inhibition was identical in both F1Fo membrane preparations as well as in isolated purified F1. In all cases inhibition was reversible. Interestingly, resveratrol and piceatannol inhibited both ATPase and ATP synthesis whereas quercetin, quercetrin or quercetin-3-β-d glucoside inhibited only ATPase activity and not ATP synthesis.

The role of αPhe-291 residue in phosphate binding by Escherichia coli F1F0-ATP synthase was examined. X-ray structures of bovine mitochondrial enzyme suggest that this residue resides in close proximity to the conserved βR246 residue. Herein, we show that mutations αF291D and αF291E in E. coli reduce the ATPase activity of F1F0 membranes by 350-fold. Yet, significant oxidative phosphorylation activity is retained. In contrast to wild-type, ATPase activities of mutants were not inhibited by MgADP-azide, MgADP-fluoroaluminate, or MgADP-fluoroscandium. Whereas, 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole (NBD-Cl) inhibited wild-type ATPase essentially completely, ATPase in mutants was inhibited maximally by ∼75%, although reaction still occurred at residue βTyr-297, proximal to αPhe-291 in the phosphate-binding pocket. Inhibition characteristics supported the conclusion that NBD-Cl reacts in βE (empty) catalytic sites, as shown previously by X-ray structure analysis. Phosphate protected against NBD-Cl inhibition in wild-type but not in mutants. In addition, our data suggest that the interaction of αPhe-291 with phosphate during ATP hydrolysis or synthesis may be distinct.

We have studied the inhibitory effect of natural and structurally modified polyphenols on Escherichia coli ATP synthase to test (I) if the beneficial dietary effects of polyphenols are related to their inhibitory actions on ATP synthase, (II) if inhibitory effects of polyphenolic compound could be augmented through structural modifications, and (III) if they can act as antimicrobial agent through their actions on ATP synthesis. X-ray crystal structures of polyphenol binding sites suggested that polyphenols bind at a distinct polyphenol binding pocket, at the interface of α,β,γ-subunits. We found that both natural and modified polyphenols inhibit E. coli ATP synthase to varying degrees and structural modifications resulted in augmented inhibition. Inhibition was reversible in all cases. Both natural and modulated compounds inhibited E. coli cell growth to varying degrees. We conclude that dietary benefits of polyphenols may be in part due to the inhibition of ATP synthase.

ATP Synthase is the fundamental means of cellular energy production in animals, plants, and almost all microorganisms. In order to understand the mechanism of ATP catalysis, critical amino acid residues involved in Pi binding have to be identified. The αVISIT-DG sequence at the interface of α/β subunits that contains residues from 345-351 is highly conserved and αAsp-350 has been chosen because of its negative charge side chain and its close proximity (~2.8 Å) to the known phosphate binding residue αArg-376. The mutant's αD350R, αD350Q, αD350A, αR376A/D, and αG351R/A/D were generated by site directed mutagenesis and several biochemical assays were performed on them to understand the role played by the amino acid residues in Pi binding. Biochemical results suggest that αD350 may be involved in catalysis of ATP synthase and play an important role in Pi binding, whereas αG351 may be involved only in the structural integrity.