@article{1423, abstract = {Direct reciprocity is a mechanism for the evolution of cooperation based on repeated interactions. When individuals meet repeatedly, they can use conditional strategies to enforce cooperative outcomes that would not be feasible in one-shot social dilemmas. Direct reciprocity requires that individuals keep track of their past interactions and find the right response. However, there are natural bounds on strategic complexity: Humans find it difficult to remember past interactions accurately, especially over long timespans. Given these limitations, it is natural to ask how complex strategies need to be for cooperation to evolve. Here, we study stochastic evolutionary game dynamics in finite populations to systematically compare the evolutionary performance of reactive strategies, which only respond to the co-player's previous move, and memory-one strategies, which take into account the own and the co-player's previous move. In both cases, we compare deterministic strategy and stochastic strategy spaces. For reactive strategies and small costs, we find that stochasticity benefits cooperation, because it allows for generous-tit-for-tat. For memory one strategies and small costs, we find that stochasticity does not increase the propensity for cooperation, because the deterministic rule of win-stay, lose-shift works best. For memory one strategies and large costs, however, stochasticity can augment cooperation.}, author = {Baek, Seung and Jeong, Hyeongchai and Hilbe, Christian and Nowak, Martin}, journal = {Scientific Reports}, publisher = {Nature Publishing Group}, title = {{Comparing reactive and memory-one strategies of direct reciprocity}}, doi = {10.1038/srep25676}, volume = {6}, year = {2016}, } @article{1426, abstract = {Brood parasites exploit their host in order to increase their own fitness. Typically, this results in an arms race between parasite trickery and host defence. Thus, it is puzzling to observe hosts that accept parasitism without any resistance. The ‘mafia’ hypothesis suggests that these hosts accept parasitism to avoid retaliation. Retaliation has been shown to evolve when the hosts condition their response to mafia parasites, who use depredation as a targeted response to rejection. However, it is unclear if acceptance would also emerge when ‘farming’ parasites are present in the population. Farming parasites use depredation to synchronize the timing with the host, destroying mature clutches to force the host to re-nest. Herein, we develop an evolutionary model to analyse the interaction between depredatory parasites and their hosts. We show that coevolutionary cycles between farmers and mafia can still induce host acceptance of brood parasites. However, this equilibrium is unstable and in the long-run the dynamics of this host–parasite interaction exhibits strong oscillations: when farmers are the majority, accepters conditional to mafia (the host will reject first and only accept after retaliation by the parasite) have a higher fitness than unconditional accepters (the host always accepts parasitism). This leads to an increase in mafia parasites’ fitness and in turn induce an optimal environment for accepter hosts.}, author = {Chakra, Maria and Hilbe, Christian and Traulsen, Arne}, journal = {Royal Society Open Science}, number = {5}, publisher = {Royal Society, The}, title = {{Coevolutionary interactions between farmers and mafia induce host acceptance of avian brood parasites}}, doi = {10.1098/rsos.160036}, volume = {3}, year = {2016}, } @article{1427, abstract = {Changes in gene expression are an important mode of evolution; however, the proximate mechanism of these changes is poorly understood. In particular, little is known about the effects of mutations within cis binding sites for transcription factors, or the nature of epistatic interactions between these mutations. Here, we tested the effects of single and double mutants in two cis binding sites involved in the transcriptional regulation of the Escherichia coli araBAD operon, a component of arabinose metabolism, using a synthetic system. This system decouples transcriptional control from any posttranslational effects on fitness, allowing a precise estimate of the effect of single and double mutations, and hence epistasis, on gene expression. We found that epistatic interactions between mutations in the araBAD cis-regulatory element are common, and that the predominant form of epistasis is negative. The magnitude of the interactions depended on whether the mutations are located in the same or in different operator sites. Importantly, these epistatic interactions were dependent on the presence of arabinose, a native inducer of the araBAD operon in vivo, with some interactions changing in sign (e.g., from negative to positive) in its presence. This study thus reveals that mutations in even relatively simple cis-regulatory elements interact in complex ways such that selection on the level of gene expression in one environment might perturb regulation in the other environment in an unpredictable and uncorrelated manner.}, author = {Lagator, Mato and Igler, Claudia and Moreno, Anaisa and Guet, Calin C and Bollback, Jonathan P}, journal = {Molecular Biology and Evolution}, number = {3}, pages = {761 -- 769}, publisher = {Oxford University Press}, title = {{Epistatic interactions in the arabinose cis-regulatory element}}, doi = {10.1093/molbev/msv269}, volume = {33}, year = {2016}, } @inproceedings{1428, abstract = {We report on a mathematically rigorous analysis of the superfluid properties of a Bose- Einstein condensate in the many-body ground state of a one-dimensional model of interacting bosons in a random potential.}, author = {Könenberg, Martin and Moser, Thomas and Seiringer, Robert and Yngvason, Jakob}, booktitle = {Journal of Physics: Conference Series}, location = {Shanghai, China}, number = {1}, publisher = {IOP Publishing Ltd.}, title = {{Superfluidity and BEC in a Model of Interacting Bosons in a Random Potential}}, doi = {10.1088/1742-6596/691/1/012016}, volume = {691}, year = {2016}, } @article{1429, abstract = {Solitons are localized waves formed by a balance of focusing and defocusing effects. These nonlinear waves exist in diverse forms of matter yet exhibit similar properties including stability, periodic recurrence and particle-like trajectories. One important property is soliton fission, a process by which an energetic higher-order soliton breaks apart due to dispersive or nonlinear perturbations. Here we demonstrate through both experiment and theory that nonlinear photocarrier generation can induce soliton fission. Using near-field measurements, we directly observe the nonlinear spatial and temporal evolution of optical pulses in situ in a nanophotonic semiconductor waveguide. We develop an analytic formalism describing the free-carrier dispersion (FCD) perturbation and show the experiment exceeds the minimum threshold by an order of magnitude. We confirm these observations with a numerical nonlinear Schrödinger equation model. These results provide a fundamental explanation and physical scaling of optical pulse evolution in free-carrier media and could enable improved supercontinuum sources in gas based and integrated semiconductor waveguides.}, author = {Husko, Chad and Wulf, Matthias and Lefrançois, Simon and Combrié, Sylvain and Lehoucq, Gaëlle and De Rossi, Alfredo and Eggleton, Benjamin and Kuipers, Laurens}, journal = {Nature Communications}, publisher = {Nature Publishing Group}, title = {{Free-carrier-induced soliton fission unveiled by in situ measurements in nanophotonic waveguides}}, doi = {10.1038/ncomms11332}, volume = {7}, year = {2016}, } @article{9456, abstract = {The discovery of introns four decades ago was one of the most unexpected findings in molecular biology. Introns are sequences interrupting genes that must be removed as part of messenger RNA production. Genome sequencing projects have shown that most eukaryotic genes contain at least one intron, and frequently many. Comparison of these genomes reveals a history of long evolutionary periods during which few introns were gained, punctuated by episodes of rapid, extensive gain. However, although several detailed mechanisms for such episodic intron generation have been proposed, none has been empirically supported on a genomic scale. Here we show how short, non-autonomous DNA transposons independently generated hundreds to thousands of introns in the prasinophyte Micromonas pusilla and the pelagophyte Aureococcus anophagefferens. Each transposon carries one splice site. The other splice site is co-opted from the gene sequence that is duplicated upon transposon insertion, allowing perfect splicing out of the RNA. The distributions of sequences that can be co-opted are biased with respect to codons, and phasing of transposon-generated introns is similarly biased. These transposons insert between pre-existing nucleosomes, so that multiple nearby insertions generate nucleosome-sized intervening segments. Thus, transposon insertion and sequence co-option may explain the intron phase biases and prevalence of nucleosome-sized exons observed in eukaryotes. Overall, the two independent examples of proliferating elements illustrate a general DNA transposon mechanism that can plausibly account for episodes of rapid, extensive intron gain during eukaryotic evolution.}, author = {Huff, Jason T. and Zilberman, Daniel and Roy, Scott W.}, issn = {1476-4687}, journal = {Nature}, number = {7626}, pages = {533--536}, publisher = {Springer Nature }, title = {{Mechanism for DNA transposons to generate introns on genomic scales}}, doi = {10.1038/nature20110}, volume = {538}, year = {2016}, } @article{9473, abstract = {Cytosine DNA methylation regulates the expression of eukaryotic genes and transposons. Methylation is copied by methyltransferases after DNA replication, which results in faithful transmission of methylation patterns during cell division and, at least in flowering plants, across generations. Transgenerational inheritance is mediated by a small group of cells that includes gametes and their progenitors. However, methylation is usually analyzed in somatic tissues that do not contribute to the next generation, and the mechanisms of transgenerational inheritance are inferred from such studies. To gain a better understanding of how DNA methylation is inherited, we analyzed purified Arabidopsis thaliana sperm and vegetative cells-the cell types that comprise pollen-with mutations in the DRM, CMT2, and CMT3 methyltransferases. We find that DNA methylation dependency on these enzymes is similar in sperm, vegetative cells, and somatic tissues, although DRM activity extends into heterochromatin in vegetative cells, likely reflecting transcription of heterochromatic transposons in this cell type. We also show that lack of histone H1, which elevates heterochromatic DNA methylation in somatic tissues, does not have this effect in pollen. Instead, levels of CG methylation in wild-type sperm and vegetative cells, as well as in wild-type microspores from which both pollen cell types originate, are substantially higher than in wild-type somatic tissues and similar to those of H1-depleted roots. Our results demonstrate that the mechanisms of methylation maintenance are similar between pollen and somatic cells, but the efficiency of CG methylation is higher in pollen, allowing methylation patterns to be accurately inherited across generations.}, author = {Hsieh, Ping-Hung and He, Shengbo and Buttress, Toby and Gao, Hongbo and Couchman, Matthew and Fischer, Robert L. and Zilberman, Daniel and Feng, Xiaoqi}, issn = {1091-6490}, journal = {Proceedings of the National Academy of Sciences}, number = {52}, pages = {15132--15137}, publisher = {National Academy of Sciences}, title = {{Arabidopsis male sexual lineage exhibits more robust maintenance of CG methylation than somatic tissues}}, doi = {10.1073/pnas.1619074114}, volume = {113}, year = {2016}, } @article{9477, abstract = {Cytosine methylation is a DNA modification with important regulatory functions in eukaryotes. In flowering plants, sexual reproduction is accompanied by extensive DNA demethylation, which is required for proper gene expression in the endosperm, a nutritive extraembryonic seed tissue. Endosperm arises from a fusion of a sperm cell carried in the pollen and a female central cell. Endosperm DNA demethylation is observed specifically on the chromosomes inherited from the central cell in Arabidopsis thaliana, rice, and maize, and requires the DEMETER DNA demethylase in Arabidopsis. DEMETER is expressed in the central cell before fertilization, suggesting that endosperm demethylation patterns are inherited from the central cell. Down-regulation of the MET1 DNA methyltransferase has also been proposed to contribute to central cell demethylation. However, with the exception of three maize genes, central cell DNA methylation has not been directly measured, leaving the origin and mechanism of endosperm demethylation uncertain. Here, we report genome-wide analysis of DNA methylation in the central cells of Arabidopsis and rice—species that diverged 150 million years ago—as well as in rice egg cells. We find that DNA demethylation in both species is initiated in central cells, which requires DEMETER in Arabidopsis. However, we do not observe a global reduction of CG methylation that would be indicative of lowered MET1 activity; on the contrary, CG methylation efficiency is elevated in female gametes compared with nonsexual tissues. Our results demonstrate that locus-specific, active DNA demethylation in the central cell is the origin of maternal chromosome hypomethylation in the endosperm.}, author = {Park, Kyunghyuk and Kim, M. Yvonne and Vickers, Martin and Park, Jin-Sup and Hyun, Youbong and Okamoto, Takashi and Zilberman, Daniel and Fischer, Robert L. and Feng, Xiaoqi and Choi, Yeonhee and Scholten, Stefan}, issn = {1091-6490}, journal = {Proceedings of the National Academy of Sciences}, keywords = {Multidisciplinary}, number = {52}, pages = {15138--15143}, publisher = {National Academy of Sciences}, title = {{DNA demethylation is initiated in the central cells of Arabidopsis and rice}}, doi = {10.1073/pnas.1619047114}, volume = {113}, year = {2016}, } @inproceedings{948, abstract = {Experience constantly shapes neural circuits through a variety of plasticity mechanisms. While the functional roles of some plasticity mechanisms are well-understood, it remains unclear how changes in neural excitability contribute to learning. Here, we develop a normative interpretation of intrinsic plasticity (IP) as a key component of unsupervised learning. We introduce a novel generative mixture model that accounts for the class-specific statistics of stimulus intensities, and we derive a neural circuit that learns the input classes and their intensities. We will analytically show that inference and learning for our generative model can be achieved by a neural circuit with intensity-sensitive neurons equipped with a specific form of IP. Numerical experiments verify our analytical derivations and show robust behavior for artificial and natural stimuli. Our results link IP to non-trivial input statistics, in particular the statistics of stimulus intensities for classes to which a neuron is sensitive. More generally, our work paves the way toward new classification algorithms that are robust to intensity variations.}, author = {Monk, Travis and Savin, Cristina and Lücke, Jörg}, location = {Barcelona, Spaine}, pages = {4285 -- 4293}, publisher = {Neural Information Processing Systems}, title = {{Neurons equipped with intrinsic plasticity learn stimulus intensity statistics}}, volume = {29}, year = {2016}, } @article{1008, abstract = {Feedback loops in biological networks, among others, enable differentiation and cell cycle progression, and increase robustness in signal transduction. In natural networks, feedback loops are often complex and intertwined, making it challenging to identify which loops are mainly responsible for an observed behavior. However, minimal synthetic replicas could allow for such identification. Here, we engineered a synthetic permease-inducer-repressor system in Saccharomyces cerevisiae to analyze if a transport-mediated positive feedback loop could be a core mechanism for the switch-like behavior in the regulation of metabolic gene networks such as the S. cerevisiae GAL system or the Escherichia coli lac operon. We characterized the synthetic circuit using deterministic and stochastic mathematical models. Similar to its natural counterparts, our synthetic system shows bistable and hysteretic behavior, and the inducer concentration range for bistability as well as the switching rates between the two stable states depend on the repressor concentration. Our results indicate that a generic permease–inducer–repressor circuit with a single feedback loop is sufficient to explain the experimentally observed bistable behavior of the natural systems. We anticipate that the approach of reimplementing natural systems with orthogonal parts to identify crucial network components is applicable to other natural systems such as signaling pathways.}, author = {Gnügge, Robert and Dharmarajan, Lekshmi and Lang, Moritz and Stelling, Jörg}, journal = {ACS Synthetic Biology}, number = {10}, pages = {1098 -- 1107}, publisher = {American Chemical Society}, title = {{An orthogonal permease–inducer–repressor feedback loop shows bistability}}, doi = {10.1021/acssynbio.6b00013}, volume = {5}, year = {2016}, } @article{1181, abstract = {This review accompanies a 2016 SFN mini-symposium presenting examples of current studies that address a central question: How do neural stem cells (NSCs) divide in different ways to produce heterogeneous daughter types at the right time and in proper numbers to build a cerebral cortex with the appropriate size and structure? We will focus on four aspects of corticogenesis: cytokinesis events that follow apical mitoses of NSCs; coordinating abscission with delamination from the apical membrane; timing of neurogenesis and its indirect regulation through emergence of intermediate progenitors; and capacity of single NSCs to generate the correct number and laminar fate of cortical neurons. Defects in these mechanisms can cause microcephaly and other brain malformations, and understanding them is critical to designing diagnostic tools and preventive and corrective therapies.}, author = {Dwyer, Noelle and Chen, Bin and Chou, Shen and Hippenmeyer, Simon and Nguyen, Laurent and Ghashghaei, Troy}, journal = {Journal of Neuroscience}, number = {45}, pages = {11394 -- 11401}, publisher = {Society for Neuroscience}, title = {{Neural stem cells to cerebral cortex: Emerging mechanisms regulating progenitor behavior and productivity}}, doi = {10.1523/JNEUROSCI.2359-16.2016}, volume = {36}, year = {2016}, } @inproceedings{1182, abstract = {Balanced knockout tournaments are ubiquitous in sports competitions and are also used in decisionmaking and elections. The traditional computational question, that asks to compute a draw (optimal draw) that maximizes the winning probability for a distinguished player, has received a lot of attention. Previous works consider the problem where the pairwise winning probabilities are known precisely, while we study how robust is the winning probability with respect to small errors in the pairwise winning probabilities. First, we present several illuminating examples to establish: (a) there exist deterministic tournaments (where the pairwise winning probabilities are 0 or 1) where one optimal draw is much more robust than the other; and (b) in general, there exist tournaments with slightly suboptimal draws that are more robust than all the optimal draws. The above examples motivate the study of the computational problem of robust draws that guarantee a specified winning probability. Second, we present a polynomial-time algorithm for approximating the robustness of a draw for sufficiently small errors in pairwise winning probabilities, and obtain that the stated computational problem is NP-complete. We also show that two natural cases of deterministic tournaments where the optimal draw could be computed in polynomial time also admit polynomial-time algorithms to compute robust optimal draws.}, author = {Chatterjee, Krishnendu and Ibsen-Jensen, Rasmus and Tkadlec, Josef}, location = {New York, NY, USA}, pages = {172 -- 179}, publisher = {AAAI Press}, title = {{Robust draws in balanced knockout tournaments}}, volume = {2016-January}, year = {2016}, } @article{1183, abstract = {Autism spectrum disorders (ASD) are a group of genetic disorders often overlapping with other neurological conditions. We previously described abnormalities in the branched-chain amino acid (BCAA) catabolic pathway as a cause of ASD. Here, we show that the solute carrier transporter 7a5 (SLC7A5), a large neutral amino acid transporter localized at the blood brain barrier (BBB), has an essential role in maintaining normal levels of brain BCAAs. In mice, deletion of Slc7a5 from the endothelial cells of the BBB leads to atypical brain amino acid profile, abnormal mRNA translation, and severe neurological abnormalities. Furthermore, we identified several patients with autistic traits and motor delay carrying deleterious homozygous mutations in the SLC7A5 gene. Finally, we demonstrate that BCAA intracerebroventricular administration ameliorates abnormal behaviors in adult mutant mice. Our data elucidate a neurological syndrome defined by SLC7A5 mutations and support an essential role for the BCAA in human brain function.}, author = {Tarlungeanu, Dora-Clara and Deliu, Elena and Dotter, Christoph and Kara, Majdi and Janiesch, Philipp and Scalise, Mariafrancesca and Galluccio, Michele and Tesulov, Mateja and Morelli, Emanuela and Sönmez, Fatma and Bilgüvar, Kaya and Ohgaki, Ryuichi and Kanai, Yoshikatsu and Johansen, Anide and Esharif, Seham and Ben Omran, Tawfeg and Topcu, Meral and Schlessinger, Avner and Indiveri, Cesare and Duncan, Kent and Caglayan, Ahmet and Günel, Murat and Gleeson, Joseph and Novarino, Gaia}, journal = {Cell}, number = {6}, pages = {1481 -- 1494}, publisher = {Cell Press}, title = {{Impaired amino acid transport at the blood brain barrier is a cause of autism spectrum disorder}}, doi = {10.1016/j.cell.2016.11.013}, volume = {167}, year = {2016}, } @article{1184, abstract = {Across multicellular organisms, the costs of reproduction and self-maintenance result in a life history trade-off between fecundity and longevity. Queens of perennial social Hymenoptera are both highly fertile and long-lived, and thus, this fundamental trade-off is lacking. Whether social insect males similarly evade the fecundity/longevity trade-off remains largely unstudied. Wingless males of the ant genus Cardiocondyla stay in their natal colonies throughout their relatively long lives and mate with multiple female sexuals. Here, we show that Cardiocondyla obscurior males that were allowed to mate with large numbers of female sexuals had a shortened life span compared to males that mated at a low frequency or virgin males. Although frequent mating negatively affects longevity, males clearly benefit from a “live fast, die young strategy” by inseminating as many female sexuals as possible at a cost to their own survival.}, author = {Metzler, Sina and Heinze, Jürgen and Schrempf, Alexandra}, journal = {Ecology and Evolution}, number = {24}, pages = {8903 -- 8906}, publisher = {Wiley-Blackwell}, title = {{Mating and longevity in ant males}}, doi = {10.1002/ece3.2474}, volume = {6}, year = {2016}, } @article{1185, abstract = {The developmental programme of the pistil is under the control of both auxin and cytokinin. Crosstalk between these factors converges on regulation of the auxin carrier PIN-FORMED 1 (PIN1). Here, we show that in the triple transcription factor mutant cytokinin response factor 2 (crf2) crf3 crf6 both pistil length and ovule number were reduced. PIN1 expression was also lower in the triple mutant and the phenotypes could not be rescued by exogenous cytokinin application. pin1 complementation studies using genomic PIN1 constructs showed that the pistil phenotypes were only rescued when the PCRE1 domain, to which CRFs bind, was present. Without this domain, pin mutants resemble the crf2 crf3 crf6 triple mutant, indicating the pivotal role of CRFs in auxin-cytokinin crosstalk.}, author = {Cucinotta, Mara and Manrique, Silvia and Guazzotti, Andrea and Quadrelli, Nadia and Mendes, Marta and Benková, Eva and Colombo, Lucia}, journal = {Development}, number = {23}, pages = {4419 -- 4424}, publisher = {Company of Biologists}, title = {{Cytokinin response factors integrate auxin and cytokinin pathways for female reproductive organ development}}, doi = {10.1242/dev.143545}, volume = {143}, year = {2016}, } @article{1186, abstract = {The human pathogen Streptococcus pneumoniae is decorated with a special class of surface-proteins known as choline-binding proteins (CBPs) attached to phosphorylcholine (PCho) moieties from cell-wall teichoic acids. By a combination of X-ray crystallography, NMR, molecular dynamics techniques and in vivo virulence and phagocytosis studies, we provide structural information of choline-binding protein L (CbpL) and demonstrate its impact on pneumococcal pathogenesis and immune evasion. CbpL is a very elongated three-module protein composed of (i) an Excalibur Ca 2+ -binding domain -reported in this work for the very first time-, (ii) an unprecedented anchorage module showing alternate disposition of canonical and non-canonical choline-binding sites that allows vine-like binding of fully-PCho-substituted teichoic acids (with two choline moieties per unit), and (iii) a Ltp-Lipoprotein domain. Our structural and infection assays indicate an important role of the whole multimodular protein allowing both to locate CbpL at specific places on the cell wall and to interact with host components in order to facilitate pneumococcal lung infection and transmigration from nasopharynx to the lungs and blood. CbpL implication in both resistance against killing by phagocytes and pneumococcal pathogenesis further postulate this surface-protein as relevant among the pathogenic arsenal of the pneumococcus.}, author = {Gutierrez-Fernandez, Javier and Saleh, Malek and Alcorlo, Martín and Gómez Mejóa, Alejandro and Pantoja Uceda, David and Treviño, Miguel and Vob, Franziska and Abdullah, Mohammed and Galán Bartual, Sergio and Seinen, Jolien and Sánchez Murcia, Pedro and Gago, Federico and Bruix, Marta and Hammerschmidt, Sven and Hermoso, Juan}, journal = {Scientific Reports}, publisher = {Nature Publishing Group}, title = {{Modular architecture and unique teichoic acid recognition features of choline-binding protein L CbpL contributing to pneumococcal pathogenesis}}, doi = {10.1038/srep38094}, volume = {6}, year = {2016}, } @article{1188, abstract = {We consider a population dynamics model coupling cell growth to a diffusion in the space of metabolic phenotypes as it can be obtained from realistic constraints-based modelling. In the asymptotic regime of slow diffusion, that coincides with the relevant experimental range, the resulting non-linear Fokker–Planck equation is solved for the steady state in the WKB approximation that maps it into the ground state of a quantum particle in an Airy potential plus a centrifugal term. We retrieve scaling laws for growth rate fluctuations and time response with respect to the distance from the maximum growth rate suggesting that suboptimal populations can have a faster response to perturbations.}, author = {De Martino, Daniele and Masoero, Davide}, journal = { Journal of Statistical Mechanics: Theory and Experiment}, number = {12}, publisher = {IOPscience}, title = {{Asymptotic analysis of noisy fitness maximization, applied to metabolism & growth}}, doi = {10.1088/1742-5468/aa4e8f}, volume = {2016}, year = {2016}, } @inproceedings{1193, abstract = {We consider the recent formulation of the Algorithmic Lovász Local Lemma [1], [2] for finding objects that avoid "bad features", or "flaws". It extends the Moser-Tardos resampling algorithm [3] to more general discrete spaces. At each step the method picks a flaw present in the current state and "resamples" it using a "resampling oracle" provided by the user. However, it is less flexible than the Moser-Tardos method since [1], [2] require a specific flaw selection rule, whereas [3] allows an arbitrary rule (and thus can potentially be implemented more efficiently). We formulate a new "commutativity" condition, and prove that it is sufficient for an arbitrary rule to work. It also enables an efficient parallelization under an additional assumption. We then show that existing resampling oracles for perfect matchings and permutations do satisfy this condition. Finally, we generalize the precondition in [2] (in the case of symmetric potential causality graphs). This unifies special cases that previously were treated separately.}, author = {Kolmogorov, Vladimir}, booktitle = {Proceedings - Annual IEEE Symposium on Foundations of Computer Science}, location = {New Brunswick, NJ, USA }, publisher = {IEEE}, title = {{Commutativity in the algorithmic Lovasz local lemma}}, doi = {10.1109/FOCS.2016.88}, volume = {2016-December}, year = {2016}, } @article{1195, abstract = {The genetic analysis of experimentally evolving populations typically relies on short reads from pooled individuals (Pool-Seq). While this method provides reliable allele frequency estimates, the underlying haplotype structure remains poorly characterized. With small population sizes and adaptive variants that start from low frequencies, the interpretation of selection signatures in most Evolve and Resequencing studies remains challenging. To facilitate the characterization of selection targets, we propose a new approach that reconstructs selected haplotypes from replicated time series, using Pool-Seq data. We identify selected haplotypes through the correlated frequencies of alleles carried by them. Computer simulations indicate that selected haplotype-blocks of several Mb can be reconstructed with high confidence and low error rates, even when allele frequencies change only by 20% across three replicates. Applying this method to real data from D. melanogaster populations adapting to a hot environment, we identify a selected haplotype-block of 6.93 Mb. We confirm the presence of this haplotype-block in evolved populations by experimental haplotyping, demonstrating the power and accuracy of our haplotype reconstruction from Pool-Seq data. We propose that the combination of allele frequency estimates with haplotype information will provide the key to understanding the dynamics of adaptive alleles. }, author = {Franssen, Susan and Barton, Nicholas H and Schlötterer, Christian}, journal = {Molecular Biology and Evolution}, number = {1}, pages = {174 -- 184}, publisher = {Oxford University Press}, title = {{Reconstruction of haplotype-blocks selected during experimental evolution.}}, doi = {10.1093/molbev/msw210}, volume = {34}, year = {2016}, } @article{1197, abstract = {Across the nervous system, certain population spiking patterns are observed far more frequently than others. A hypothesis about this structure is that these collective activity patterns function as population codewords–collective modes–carrying information distinct from that of any single cell. We investigate this phenomenon in recordings of ∼150 retinal ganglion cells, the retina’s output. We develop a novel statistical model that decomposes the population response into modes; it predicts the distribution of spiking activity in the ganglion cell population with high accuracy. We found that the modes represent localized features of the visual stimulus that are distinct from the features represented by single neurons. Modes form clusters of activity states that are readily discriminated from one another. When we repeated the same visual stimulus, we found that the same mode was robustly elicited. These results suggest that retinal ganglion cells’ collective signaling is endowed with a form of error-correcting code–a principle that may hold in brain areas beyond retina.}, author = {Prentice, Jason and Marre, Olivier and Ioffe, Mark and Loback, Adrianna and Tkacik, Gasper and Berry, Michael}, journal = {PLoS Computational Biology}, number = {11}, publisher = {Public Library of Science}, title = {{Error-robust modes of the retinal population code}}, doi = {10.1371/journal.pcbi.1005148}, volume = {12}, year = {2016}, }