@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{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{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{1991, abstract = {Although transitions of sex-determination mechanisms are frequent in species with homomorphic sex chromosomes, heteromorphic sex chromosomes are thought to represent a terminal evolutionary stage owing to chromosome-specific adaptations such as dosage compensation or an accumulation of sex-specific mutations. Here we show that an autosome of Drosophila, the dot chromosome, was ancestrally a differentiated X chromosome. We analyse the whole genome of true fruitflies (Tephritidae), flesh flies (Sarcophagidae) and soldier flies (Stratiomyidae) to show that genes located on the dot chromosome of Drosophila are X-linked in outgroup species, whereas Drosophila X-linked genes are autosomal. We date this chromosomal transition to early drosophilid evolution by sequencing the genome of other Drosophilidae. Our results reveal several puzzling aspects of Drosophila dot chromosome biology to be possible remnants of its former life as a sex chromosome, such as its minor feminizing role in sex determination or its targeting by a chromosome-specific regulatory mechanism. We also show that patterns of biased gene expression of the dot chromosome during early embryogenesis, oogenesis and spermatogenesis resemble that of the current X chromosome. Thus, although sex chromosomes are not necessarily evolutionary end points and can revert back to an autosomal inheritance, the highly specialized genome architecture of this former X chromosome suggests that severe fitness costs must be overcome for such a turnover to occur.}, author = {Beatriz Vicoso and Bachtrog, Doris}, journal = {Nature}, number = {7458}, pages = {332 -- 335}, publisher = {Nature Publishing Group}, title = {{Reversal of an ancient sex chromosome to an autosome in Drosophila}}, doi = {10.1038/nature12235}, volume = {499}, 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}, } @article{2010, abstract = {Many algorithms for inferring causality rely heavily on the faithfulness assumption. The main justification for imposing this assumption is that the set of unfaithful distributions has Lebesgue measure zero, since it can be seen as a collection of hypersurfaces in a hypercube. However, due to sampling error the faithfulness condition alone is not sufficient for statistical estimation, and strong-faithfulness has been proposed and assumed to achieve uniform or high-dimensional consistency. In contrast to the plain faithfulness assumption, the set of distributions that is not strong-faithful has nonzero Lebesgue measure and in fact, can be surprisingly large as we show in this paper. We study the strong-faithfulness condition from a geometric and combinatorial point of view and give upper and lower bounds on the Lebesgue measure of strong-faithful distributions for various classes of directed acyclic graphs. Our results imply fundamental limitations for the PC-algorithm and potentially also for other algorithms based on partial correlation testing in the Gaussian case.}, author = {Uhler, Caroline and Raskutti, Garvesh and Bühlmann, Peter and Yu, Bin}, journal = {The Annals of Statistics}, number = {2}, pages = {436 -- 463}, publisher = {Institute of Mathematical Statistics}, title = {{Geometry of the faithfulness assumption in causal inference}}, doi = {10.1214/12-AOS1080}, volume = {41}, year = {2013}, } @article{2009, abstract = {Traditional statistical methods for confidentiality protection of statistical databases do not scale well to deal with GWAS databases especially in terms of guarantees regarding protection from linkage to external information. The more recent concept of differential privacy, introduced by the cryptographic community, is an approach which provides a rigorous definition of privacy with meaningful privacy guarantees in the presence of arbitrary external information, although the guarantees may come at a serious price in terms of data utility. Building on such notions, we propose new methods to release aggregate GWAS data without compromising an individual’s privacy. We present methods for releasing differentially private minor allele frequencies, chi-square statistics and p-values. We compare these approaches on simulated data and on a GWAS study of canine hair length involving 685 dogs. We also propose a privacy-preserving method for finding genome-wide associations based on a differentially-private approach to penalized logistic regression.}, author = {Uhler, Caroline and Slavkovic, Aleksandra and Fienberg, Stephen}, journal = {Journal of Privacy and Confidentiality }, number = {1}, pages = {137 -- 166}, publisher = {Carnegie Mellon University}, title = {{Privacy-preserving data sharing for genome-wide association studies}}, doi = {10.29012/jpc.v5i1.629}, volume = {5}, year = {2013}, } @article{2074, abstract = {Sex chromosomes originate from autosomes. The accumulation of sexually antagonistic mutations on protosex chromosomes selects for a loss of recombination and sets in motion the evolutionary processes generating heteromorphic sex chromosomes. Recombination suppression and differentiation are generally viewed as the default path of sex chromosome evolution, and the occurrence of old, homomorphic sex chromosomes, such as those of ratite birds, has remained a mystery. Here, we analyze the genome and transcriptome of emu (Dromaius novaehollandiae) and confirm that most genes on the sex chromosome are shared between the Z and W. Surprisingly, however, levels of gene expression are generally sex-biased for all sex-linked genes relative to autosomes, including those in the pseudoautosomal region, and the male-bias increases after gonad formation. This expression bias suggests that the emu sex chromosomes have become masculinized, even in the absence of ZW differentiation. Thus, birds may have taken different evolutionary solutions to minimize the deleterious effects imposed by sexually antagonistic mutations: some lineages eliminate recombination along the protosex chromosomes to physically restrict sexually antagonistic alleles to one sex, whereas ratites evolved sex-biased expression to confine the product of a sexually antagonistic allele to the sex it benefits. This difference in conflict resolution may explain the preservation of recombining, homomorphic sex chromosomes in other lineages and illustrates the importance of sexually antagonistic mutations driving the evolution of sex chromosomes. }, author = {Beatriz Vicoso and Kaiser, Vera B and Bachtrog, Doris}, journal = {PNAS}, number = {16}, pages = {6453 -- 6458}, publisher = {National Academy of Sciences}, title = {{Sex biased gene expression at homomorphic sex chromosomes in emus and its implication for sex chromosome evolution}}, doi = {10.1073/pnas.1217027110}, volume = {110}, year = {2013}, }