@article{7746, abstract = {Clutch size and egg mass are life history traits that have been extensively studied in wild bird populations, as life history theory predicts a negative trade‐off between them, either at the phenotypic or at the genetic level. Here, we analyse the genomic architecture of these heritable traits in a wild great tit (Parus major) population, using three marker‐based approaches – chromosome partitioning, quantitative trait locus (QTL) mapping and a genome‐wide association study (GWAS). The variance explained by each great tit chromosome scales with predicted chromosome size, no location in the genome contains genome‐wide significant QTL, and no individual SNPs are associated with a large proportion of phenotypic variation, all of which may suggest that variation in both traits is due to many loci of small effect, located across the genome. There is no evidence that any regions of the genome contribute significantly to both traits, which combined with a small, nonsignificant negative genetic covariance between the traits, suggests the absence of genetic constraints on the independent evolution of these traits. Our findings support the hypothesis that variation in life history traits in natural populations is likely to be determined by many loci of small effect spread throughout the genome, which are subject to continued input of variation by mutation and migration, although we cannot exclude the possibility of an additional input of major effect genes influencing either trait.}, author = {Santure, Anna W. and De Cauwer, Isabelle and Robinson, Matthew Richard and Poissant, Jocelyn and Sheldon, Ben C. and Slate, Jon}, issn = {0962-1083}, journal = {Molecular Ecology}, number = {15}, pages = {3949--3962}, publisher = {Wiley}, title = {{Genomic dissection of variation in clutch size and egg mass in a wild great tit (Parus major) population}}, doi = {10.1111/mec.12376}, volume = {22}, year = {2013}, } @article{7747, abstract = {Acquisition and allocation of resources are central to life‐history theory. However, empirical work typically focuses only on allocation despite the fact that relationships between fitness components may be governed by differences in the ability of individuals to acquire resources across environments. Here, we outline a statistical framework to partition the genetic basis of multivariate plasticity into independent axes of genetic variation, and quantify for the first time, the extent to which specific traits drive multitrait genotype–environment interactions. Our framework generalises to analyses of plasticity, growth and ageing. We apply this approach to a unique, large‐scale, multivariate study of acquisition, allocation and plasticity in the life history of the cricket, Gryllus firmus. We demonstrate that resource acquisition and allocation are genetically correlated, and that plasticity in trade‐offs between allocation to components of fitness is 90% dependent on genetic variance for total resource acquisition. These results suggest that genotype–environment effects for resource acquisition can maintain variation in life‐history components that are typically observed in the wild.}, author = {Robinson, Matthew Richard and Beckerman, Andrew P.}, issn = {1461-023X}, journal = {Ecology Letters}, number = {3}, pages = {281--290}, publisher = {Wiley}, title = {{Quantifying multivariate plasticity: Genetic variation in resource acquisition drives plasticity in resource allocation to components of life history}}, doi = {10.1111/ele.12047}, volume = {16}, year = {2013}, } @article{7774, abstract = {In 2005, Wyart et al. [Europhys. Lett., 2005, 72, 486] showed that the low frequency vibrational properties of jammed amorphous sphere packings can be understood in terms of a length scale, called l*, that diverges as the system becomes marginally unstable. Despite the tremendous success of this theory, it has been difficult to connect the counting argument that defines l* to other length scales that diverge near the jamming transition. We present an alternate derivation of l* based on the onset of rigidity. This phenomenological approach reveals the physical mechanism underlying the length scale and is relevant to a range of systems for which the original argument breaks down. It also allows us to present the first direct numerical measurement of l*.}, author = {Goodrich, Carl Peter and Ellenbroek, Wouter G. and Liu, Andrea J.}, issn = {1744-683X}, journal = {Soft Matter}, number = {46}, publisher = {Royal Society of Chemistry}, title = {{Stability of jammed packings I: The rigidity length scale}}, doi = {10.1039/c3sm51095f}, volume = {9}, year = {2013}, } @article{7775, abstract = {As a function of packing fraction at zero temperature and applied stress, an amorphous packing of spheres exhibits a jamming transition where the system is sensitive to boundary conditions even in the thermodynamic limit. Upon further compression, the system should become insensitive to boundary conditions provided it is sufficiently large. Here we explore the linear response to a large class of boundary perturbations in 2 and 3 dimensions. We consider each finite packing with periodic-boundary conditions as the basis of an infinite square or cubic lattice and study properties of vibrational modes at arbitrary wave vector. We find that the stability of such modes can be understood in terms of a competition between plane waves and the anomalous vibrational modes associated with the jamming transition; infinitesimal boundary perturbations become irrelevant for systems that are larger than a length scale that characterizes the transverse excitations. This previously identified length diverges at the jamming transition.}, author = {Schoenholz, Samuel S. and Goodrich, Carl Peter and Kogan, Oleg and Liu, Andrea J. and Nagel, Sidney R.}, issn = {1744-683X}, journal = {Soft Matter}, number = {46}, publisher = {Royal Society of Chemistry}, title = {{Stability of jammed packings II: The transverse length scale}}, doi = {10.1039/c3sm51096d}, volume = {9}, year = {2013}, } @article{7785, abstract = {Neural circuit assembly requires selection of specific cell fates, axonal trajectories, and synaptic targets. By analyzing the function of a secreted semaphorin, Sema-2b, in Drosophila olfactory receptor neuron (ORN) development, we identified multiple molecular and cellular mechanisms that link these events. Notch signaling limits Sema-2b expression to ventromedial ORN classes, within which Sema-2b cell-autonomously sensitizes ORN axons to external semaphorins. Central-brain-derived Sema-2a and Sema-2b attract Sema-2b-expressing axons to the ventromedial trajectory. In addition, Sema-2b/PlexB-mediated axon-axon interactions consolidate this trajectory choice and promote ventromedial axon-bundle formation. Selecting the correct developmental trajectory is ultimately essential for proper target choice. These findings demonstrate that Sema-2b couples ORN axon guidance to postsynaptic target neuron dendrite patterning well before the final target selection phase, and exemplify how a single guidance molecule can drive consecutive stages of neural circuit assembly with the help of sophisticated spatial and temporal regulation.}, author = {Joo, William J. and Sweeney, Lora Beatrice Jaeger and Liang, Liang and Luo, Liqun}, issn = {0896-6273}, journal = {Neuron}, number = {4}, pages = {673--686}, publisher = {Elsevier}, title = {{Linking cell fate, trajectory choice, and target selection: Genetic analysis of sema-2b in olfactory axon targeting}}, doi = {10.1016/j.neuron.2013.03.022}, volume = {78}, year = {2013}, } @article{8030, abstract = {While the plasticity of excitatory synaptic connections in the brain has been widely studied, the plasticity of inhibitory connections is much less understood. Here, we present recent experimental and theoretical findings concerning the rules of spike timing-dependent inhibitory plasticity and their putative network function. This is a summary of a workshop at the COSYNE conference 2012.}, author = {Vogels, Tim P and Froemke, R. C. and Doyon, N. and Gilson, M. and Haas, J. S. and Liu, R. and Maffei, A. and Miller, P. and Wierenga, C. J. and Woodin, M. A. and Zenke, F. and Sprekeler, H.}, issn = {1662-5110}, journal = {Frontiers in Neural Circuits}, publisher = {Frontiers Media}, title = {{Inhibitory synaptic plasticity: Spike timing-dependence and putative network function}}, doi = {10.3389/fncir.2013.00119}, volume = {7}, year = {2013}, } @article{810, abstract = {Cryo-electron tomography combined with image processing by sub-tomogram averaging is unique in its power to resolve the structures of proteins and macromolecular complexes in situ. Limitations of the method, including the low signal to noise ratio within individual images from cryo-tomographic datasets and difficulties in determining the defocus at which the data was collected, mean that to date the very best structures obtained by sub-tomogram averaging are limited to a resolution of approximately 15. Å. Here, by optimizing data collection and defocus determination steps, we have determined the structure of assembled Mason-Pfizer monkey virus Gag protein using sub-tomogram averaging to a resolution of 8.5. Å. At this resolution alpha-helices can be directly and clearly visualized. These data demonstrate for the first time that high-resolution structural information can be obtained from cryo-electron tomograms using sub-tomogram averaging. Sub-tomogram averaging has the potential to allow detailed studies of unsolved and biologically relevant structures under biologically relevant conditions.}, author = {Florian Schur and Hagen, Wim J and De Marco, Alex and Briggs, John A}, journal = {Journal of Structural Biology}, number = {3}, pages = {394 -- 400}, publisher = {Academic Press}, title = {{Determination of protein structure at 8.5Å resolution using cryo-electron tomography and sub-tomogram averaging}}, doi = {10.1016/j.jsb.2013.10.015}, volume = {184}, year = {2013}, } @article{811, abstract = {Cell migration is commonly accompanied by protrusion of membrane ruffles and lamellipodia. In two-dimensional migration, protrusion of these thin sheets of cytoplasm is considered relevant to both exploration of new space and initiation of nascent adhesion to the substratum. Lamellipodium formation can be potently stimulated by Rho GTPases of the Rac subfamily, but alsoby RhoG or Cdc42. Here we describe viable fibroblast cell lines geneticallydeficient for Rac1 that lack detectable levels of Rac2 and Rac3. Rac-deficient cells were devoid of apparent lamellipodia, but these structures were restored by expression of either Rac subfamily member, but not by Cdc42 or RhoG. Cells deficient in Rac showed strong reduction in wound closure and random cell migration and a notable loss of sensitivity to a chemotactic gradient. Despite these defects, Rac-deficient cells were able to spread, formed filopodia and established focal adhesions. Spreading in these cells was achieved by the extension of filopodia followed by the advancement of cytoplasmic veils between them. The number and size of focal adhesions as well as their intensity were largely unaffected by genetic removal of Rac1. However, Rac deficiency increased the mobility of different components in focal adhesions, potentially explaining how Rac - although not essential - can contribute to focal adhesion assembly. Together, our data demonstrate that Rac signaling is essential for lamellipodium protrusion and for efficient cell migration, but not for spreading or filopodium formation. Our findings also suggest that Rac GTPases are crucial to the establishment or maintenance of polarity in chemotactic migration.}, author = {Steffen, Anika and Ladwein, Markus and Georgi Dimchev and Hein, Anke and Schwenkmezger, Lisa and Arens, Stefan and Ladwein, Kathrin I and Holleboom, J. Margit and Florian Schur and Small, John V and Schwarz, Janett and Gerhard, Ralf and Faix, Jan and Stradal, Theresia E and Brakebusch, Cord H and Rottner, Klemens}, journal = {Journal of Cell Science}, number = {20}, pages = {4572 -- 4588}, publisher = {Company of Biologists}, title = {{Rac function is crucial for cell migration but is not required for spreading and focal adhesion formation}}, doi = {10.1242/jcs.118232}, volume = {126}, year = {2013}, } @article{812, abstract = {Lamellipodia are sheet-like protrusions formed during migration or phagocytosis and comprise a network of actin filaments. Filament formation in this network is initiated by nucleation/branching through the actin-related protein 2/3 (Arp2/3) complex downstream of its activator, suppressor of cAMP receptor/WASP-family verprolin homologous (Scar/WAVE), but the relative relevance of Arp2/3-mediated branching versus actin filament elongation is unknown. Here we use instantaneous interference with Arp2/3 complex function in live fibroblasts with established lamellipodia. This allows direct examination of both the fate of elongating filaments upon instantaneous suppression of Arp2/3 complex activity and the consequences of this treatment on the dynamics of other lamellipodial regulators. We show that Arp2/3 complex is an essential organizer of treadmilling actin filament arrays but has little effect on the net rate of actin filament turnover at the cell periphery. In addition, Arp2/3 complex serves as key upstream factor for the recruitment of modulators of lamellipodia formation such as capping protein or cofilin. Arp2/3 complex is thus decisive for filament organization and geometry within the network not only by generating branches and novel filament ends, but also by directing capping or severing activities to the lamellipodium. Arp2/3 complex is also crucial to lamellipodia-based migration of keratocytes.}, author = {Koestler, Stefan A and Steffen, Anika and Maria Nemethova and Winterhoff, Moritz and Luo, Ningning and Holleboom, J. Margit and Krupp, Jessica and Jacob, Sonja and Vinzenz, Marlene and Florian Schur and Schlüter, Kai and Gunning, Peter W and Winkler, Christoph and Schmeiser, Christian and Faix, Jan and Stradal, Theresia E and Small, John V and Rottner, Klemens}, journal = {Molecular Biology of the Cell}, number = {18}, pages = {2861 -- 2875}, publisher = {American Society for Biology}, title = {{Arp2/3 complex is essential for actin network treadmilling as well as for targeting of capping protein and cofilin}}, doi = {10.1091/mbc.E12-12-0857}, volume = {24}, year = {2013}, } @article{1726, abstract = {The development of a functional tissue requires coordination of the amplification of progenitors and their differentiation into specific cell types. The molecular basis for this coordination during myotome ontogeny is not well understood. Dermomytome progenitors that colonize the myotome first acquire myocyte identity and subsequently proliferate as Pax7-expressing progenitors before undergoing terminal differentiation. We show that the dynamics of sonic hedgehog (Shh) signaling is crucial for this transition in both avian and mouse embryos. Initially, Shh ligand emanating from notochord/floor plate reaches the dermomyotome, where it both maintains the proliferation of dermomyotome cells and promotes myogenic differentiation of progenitors that colonized the myotome. Interfering with Shh signaling at this stage produces small myotomes and accumulation of Pax7-expressing progenitors. An in vivo reporter of Shh activity combined with mouse genetics revealed the existence of both activator and repressor Shh activities operating on distinct subsets of cells during the epaxial myotomal maturation. In contrast to observations in mice, in avians Shh promotes the differentiation of both epaxial and hypaxial myotome domains. Subsequently, myogenic progenitors become refractory to Shh; this is likely to occur at the level of, or upstream of, smoothened signaling. The end of responsiveness to Shh coincides with, and is thus likely to enable, the transition into the growth phase of the myotome.}, author = {Kahane, Nitza and Ribes, Vanessa and Anna Kicheva and Briscoe, James and Kalcheim, Chaya}, journal = {Development}, number = {8}, pages = {1740 -- 1750}, publisher = {Company of Biologists}, title = {{The transition from differentiation to growth during dermomyotome-derived myogenesis depends on temporally restricted hedgehog signaling}}, doi = {10.1242/dev.092726}, volume = {140}, year = {2013}, } @article{1727, abstract = {Cells at different positions in a developing tissue receive different concentrations of signaling molecules, called morphogens, and this influences their cell fate. Morphogen concentration gradients have been proposed to control patterning as well as growth in many developing tissues. Some outstanding questions about tissue patterning by morphogen gradients are the following: What are the mechanisms that regulate gradient formation and shape? Is the positional information encoded in the gradient sufficiently precise to determine the positions of target gene domain boundaries? What are the temporal dynamics of gradients and how do they relate to patterning and growth? These questions are inherently quantitative in nature and addressing them requires measuring morphogen concentrations in cells, levels of downstream signaling activity, and kinetics of morphogen transport. Here we first present methods for quantifying morphogen gradient shape in which the measurements can be calibrated to reflect actual morphogen concentrations. We then discuss using fluorescence recovery after photobleaching to study the kinetics of morphogen transport at the tissue level. Finally, we present particle tracking as a method to study morphogen intracellular trafficking.}, author = {Anna Kicheva and Holtzer, Laurent and Wartlick, Ortrud and Schmidt, Thomas S and González-Gaitán, Marcos A}, journal = {Cold Spring Harbor Protocols}, number = {5}, pages = {387 -- 403}, publisher = {Cold Spring Harbor Laboratory Press}, title = {{Quantitative imaging of morphogen gradients in drosophila imaginal discs}}, doi = {10.1101/pdb.top074237}, volume = {8}, year = {2013}, } @article{1759, abstract = {We report an electric-field-induced giant modulation of the hole g factor in SiGe nanocrystals. The observed effect is ascribed to a so-far overlooked contribution to the g factor that stems from the mixing between heavy- and light-hole wave functions. We show that the relative displacement between the confined heavy- and light-hole states, occurring upon application of the electric field, alters their mixing strength leading to a strong nonmonotonic modulation of the g factor.}, author = {Ares, Natalia and Golovach, Vitaly N and Georgios Katsaros and Stoffel, Mathieu and Fournel, Frank and Glazman, Leonid I and Schmidt, Oliver G and De Franceschi, Silvano}, journal = {Physical Review Letters}, number = {4}, publisher = {American Physical Society}, title = {{Nature of tunable hole g factors in quantum dots}}, doi = {10.1103/PhysRevLett.110.046602}, volume = {110}, year = {2013}, } @article{1760, abstract = {We report on hole g-factor measurements in three terminal SiGe self-assembled quantum dot devices with a top gate electrode positioned very close to the nanostructure. Measurements of both the perpendicular as well as the parallel g-factor reveal significant changes for a small modulation of the top gate voltage. From the observed modulations, we estimate that, for realistic experimental conditions, hole spins can be electrically manipulated with Rabi frequencies in the order of 100 MHz. This work emphasises the potential of hole-based nano-devices for efficient spin manipulation by means of the g-tensor modulation technique.}, author = {Ares, Natalia and Georgios Katsaros and Golovach, Vitaly N and Zhang, Jianjun and Prager, Aaron A and Glazman, Leonid I and Schmidt, Oliver G and De Franceschi, Silvano}, journal = {Applied Physics Letters}, number = {26}, publisher = {American Institute of Physics}, title = {{SiGe quantum dots for fast hole spin Rabi oscillations}}, doi = {10.1063/1.4858959}, volume = {103}, year = {2013}, } @article{1785, abstract = {The geometric aspects of quantum mechanics are emphasized most prominently by the concept of geometric phases, which are acquired whenever a quantum system evolves along a path in Hilbert space, that is, the space of quantum states of the system. The geometric phase is determined only by the shape of this path and is, in its simplest form, a real number. However, if the system has degenerate energy levels, then matrix-valued geometric state transformations, known as non-Abelian holonomies-the effect of which depends on the order of two consecutive paths-can be obtained. They are important, for example, for the creation of synthetic gauge fields in cold atomic gases or the description of non-Abelian anyon statistics. Moreover, there are proposals to exploit non-Abelian holonomic gates for the purposes of noise-resilient quantum computation. In contrast to Abelian geometric operations, non-Abelian ones have been observed only in nuclear quadrupole resonance experiments with a large number of spins, and without full characterization of the geometric process and its non-commutative nature. Here we realize non-Abelian non-adiabatic holonomic quantum operations on a single, superconducting, artificial three-level atom by applying a well-controlled, two-tone microwave drive. Using quantum process tomography, we determine fidelities of the resulting non-commuting gates that exceed 95 per cent. We show that two different quantum gates, originating from two distinct paths in Hilbert space, yield non-equivalent transformations when applied in different orders. This provides evidence for the non-Abelian character of the implemented holonomic quantum operations. In combination with a non-trivial two-quantum-bit gate, our method suggests a way to universal holonomic quantum computing.}, author = {Abdumalikov, Abdufarrukh A and Johannes Fink and Juliusson, K and Pechal, M and Berger, Stefan T and Wallraff, Andreas and Filipp, Stefan}, journal = {Nature}, number = {7446}, pages = {482 -- 485}, publisher = {Nature Publishing Group}, title = {{Experimental realization of non-Abelian non-adiabatic geometric gates}}, doi = {10.1038/nature12010}, volume = {496}, year = {2013}, } @article{1786, abstract = {We report the experimental observation and a theoretical explanation of collective suppression of linewidths for multiple superconducting qubits coupled to a good cavity. This demonstrates how strong qubit-cavity coupling can significantly modify the dephasing and dissipation processes that might be expected for individual qubits, and can potentially improve coherence times in many-body circuit QED.}, author = {Nissen, Felix and Johannes Fink and Mlynek, Jonas A and Wallraff, Andreas and Keeling, Jonathan M}, journal = {Physical Review Letters}, number = {20}, publisher = {American Physical Society}, title = {{Collective suppression of linewidths in circuit QED}}, doi = {10.1103/PhysRevLett.110.203602}, volume = {110}, year = {2013}, } @article{1787, abstract = {When two indistinguishable single photons impinge at the two inputs of a beam splitter they coalesce into a pair of photons appearing in either one of its two outputs. This effect is due to the bosonic nature of photons and was first experimentally observed by Hong, Ou and Mandel. Here, we present the observation of the Hong-Ou-Mandel effect with two independent single-photon sources in the microwave frequency domain. We probe the indistinguishability of single photons, created with a controllable delay, in time-resolved second-order cross- and auto-correlation function measurements. Using quadrature amplitude detection we are able to resolve different photon numbers and detect coherence in and between the output arms. This scheme allows us to fully characterize the two-mode entanglement of the spatially separated beam-splitter output modes. Our experiments constitute a first step towards using two-photon interference at microwave frequencies for quantum communication and information processing.}, author = {Lang, C and Eichler, Christopher and Steffen, L. Kraig and Johannes Fink and Woolley, Matthew J and Blais, Alexandre and Wallraff, Andreas}, journal = {Nature Physics}, number = {6}, pages = {345 -- 348}, publisher = {Nature Publishing Group}, title = {{Correlations, indistinguishability and entanglement in Hong-Ou-Mandel experiments at microwave frequencies}}, doi = {10.1038/nphys2612}, volume = {9}, year = {2013}, } @article{1790, abstract = {In the September 12, 2013 issue of Nature, the Epi4K Consortium (. Allen etal., 2013) reported sequencing 264patient trios with epileptic encephalopathies. The Consortium focused on genes exceptionally intolerant to sequence variations and found substantial interconnections with autism and intellectual disability gene networks.}, author = {Gaia Novarino and Baek, SeungTae and Gleeson, Joseph G}, journal = {Neuron}, number = {1}, pages = {9 -- 11}, publisher = {Elsevier}, title = {{The sacred disease: The puzzling genetics of epileptic disorders}}, doi = {10.1016/j.neuron.2013.09.019}, volume = {80}, year = {2013}, } @article{1977, abstract = {Complex I (NADH:ubiquinone oxidoreductase) is central to cellular energy production, being the first and largest enzyme of the respiratory chain in mitochondria. It couples electron transfer from NADH to ubiquinone with proton translocation across the inner mitochondrial membrane and is involved in a wide range of human neurodegenerative disorders. Mammalian complex I is composed of 44 different subunits, whereas the 'minimal' bacterial version contains 14 highly conserved 'core' subunits. The L-shaped assembly consists of hydrophilic and membrane domains. We have determined all known atomic structures of complex I, starting from the hydrophilic domain of Thermus thermophilus enzyme (eight subunits, nine Fe-S clusters), followed by the membrane domains of the Escherichia coli (six subunits, 55 transmembrane helices) and T. thermophilus (seven subunits, 64 transmembrane helices) enzymes, and finally culminating in a recent crystal structure of the entire intact complex I from T. thermophilus (536 kDa, 16 subunits, nine Fe-S clusters, 64 transmembrane helices). The structure suggests an unusual and unique coupling mechanism via longrange conformational changes. Determination of the structure of the entire complex was possible only through this step-by-step approach, building on from smaller subcomplexes towards the entire assembly. Large membrane proteins are notoriously difficult to crystallize, and so various non-standard and sometimes counterintuitive approaches were employed in order to achieve crystal diffraction to high resolution and solve the structures. These steps, as well as the implications from the final structure, are discussed in the present review.}, author = {Leonid Sazanov and Baradaran, Rozbeh and Efremov, Rouslan G and Berrisford, John M and Minhas, Gurdeep S}, journal = {Biochemical Society Transactions}, number = {5}, pages = {1265 -- 1271}, publisher = {Portland Press}, title = {{A long road towards the structure of respiratory complex I, a giant molecular proton pump}}, doi = {10.1042/BST20130193}, volume = {41}, year = {2013}, } @article{1978, abstract = {Complex I is the first and largest enzyme of the respiratory chain and has a central role in cellular energy production through the coupling of NADH:ubiquinone electron transfer to proton translocation. It is also implicated in many common human neurodegenerative diseases. Here, we report the first crystal structure of the entire, intact complex I (from Thermus thermophilus) at 3.3 Å resolution. The structure of the 536-kDa complex comprises 16 different subunits, with a total of 64 transmembrane helices and 9 iron-sulphur clusters. The core fold of subunit Nqo8 (ND1 in humans) is, unexpectedly, similar to a half-channel of the antiporter-like subunits. Small subunits nearby form a linked second half-channel, which completes the fourth proton-translocation pathway (present in addition to the channels in three antiporter-like subunits). The quinone-binding site is unusually long, narrow and enclosed. The quinone headgroup binds at the deep end of this chamber, near iron-sulphur cluster N2. Notably, the chamber is linked to the fourth channel by a 'funnel' of charged residues. The link continues over the entire membrane domain as a flexible central axis of charged and polar residues, and probably has a leading role in the propagation of conformational changes, aided by coupling elements. The structure suggests that a unique, out-of-the-membrane quinone-reaction chamber enables the redox energy to drive concerted long-range conformational changes in the four antiporter-like domains, resulting in translocation of four protons per cycle.}, author = {Baradaran, Rozbeh and Berrisford, John M and Minhas, Gurdeep S and Leonid Sazanov}, journal = {Nature}, number = {7438}, pages = {443 -- 448}, publisher = {Nature Publishing Group}, title = {{Crystal structure of the entire respiratory complex i}}, doi = {10.1038/nature11871}, volume = {494}, year = {2013}, } @article{1988, abstract = {The rod-shaped bacterium Escherichia coli selects the cell center as site of division with the help of the proteins MinC, MinD, and MinE. This protein system collectively oscillates between the two cell poles by alternately binding to the membrane in one of the two cell halves. This dynamic behavior, which emerges from the interaction of the ATPase MinD and its activator MinE on the cell membrane, has become a paradigm for protein self-organization. Recently, it has been found that not only the binding of MinD to the membrane, but also interactions of MinE with the membrane contribute to Min-protein self-organization. Here, we show that by accounting for this finding in a computational model, we can comprehensively describe all observed Min-protein patterns in vivo and in vitro. Furthermore, by varying the system's geometry, our computations predict patterns that have not yet been reported. We confirm these predictions experimentally.}, author = {Bonny, Mike and Fischer-Friedrich, Elisabeth and Martin Loose and Schwille, Petra and Kruse, Karsten}, journal = {PLoS Computational Biology}, number = {12}, publisher = {Public Library of Science}, title = {{Membrane binding of MinE allows for a comprehensive description of Min-protein pattern formation}}, doi = {10.1371/journal.pcbi.1003347}, volume = {9}, year = {2013}, }