@misc{9327, abstract = {This archive contains the missing sweater mesh animations and displacement models for the code of "Mechanics-Aware Deformation of Yarn Pattern Geometry" Code Repository: https://git.ist.ac.at/gsperl/MADYPG}, author = {Sperl, Georg and Narain, Rahul and Wojtan, Christopher J}, publisher = {IST Austria}, title = {{Mechanics-Aware Deformation of Yarn Pattern Geometry (Additional Animation/Model Data)}}, doi = {10.15479/AT:ISTA:9327}, year = {2021}, } @article{9329, abstract = {Background: To understand information coding in single neurons, it is necessary to analyze subthreshold synaptic events, action potentials (APs), and their interrelation in different behavioral states. However, detecting excitatory postsynaptic potentials (EPSPs) or currents (EPSCs) in behaving animals remains challenging, because of unfavorable signal-to-noise ratio, high frequency, fluctuating amplitude, and variable time course of synaptic events. New method: We developed a method for synaptic event detection, termed MOD (Machine-learning Optimal-filtering Detection-procedure), which combines concepts of supervised machine learning and optimal Wiener filtering. Experts were asked to manually score short epochs of data. The algorithm was trained to obtain the optimal filter coefficients of a Wiener filter and the optimal detection threshold. Scored and unscored data were then processed with the optimal filter, and events were detected as peaks above threshold. Results: We challenged MOD with EPSP traces in vivo in mice during spatial navigation and EPSC traces in vitro in slices under conditions of enhanced transmitter release. The area under the curve (AUC) of the receiver operating characteristics (ROC) curve was, on average, 0.894 for in vivo and 0.969 for in vitro data sets, indicating high detection accuracy and efficiency. Comparison with existing methods: When benchmarked using a (1 − AUC)−1 metric, MOD outperformed previous methods (template-fit, deconvolution, and Bayesian methods) by an average factor of 3.13 for in vivo data sets, but showed comparable (template-fit, deconvolution) or higher (Bayesian) computational efficacy. Conclusions: MOD may become an important new tool for large-scale, real-time analysis of synaptic activity.}, author = {Zhang, Xiaomin and Schlögl, Alois and Vandael, David H and Jonas, Peter M}, issn = {1872-678X}, journal = {Journal of Neuroscience Methods}, number = {6}, publisher = {Elsevier}, title = {{MOD: A novel machine-learning optimal-filtering method for accurate and efficient detection of subthreshold synaptic events in vivo}}, doi = {10.1016/j.jneumeth.2021.109125}, volume = {357}, year = {2021}, } @article{9330, abstract = {In nerve cells the genes encoding for α2δ subunits of voltage-gated calcium channels have been linked to synaptic functions and neurological disease. Here we show that α2δ subunits are essential for the formation and organization of glutamatergic synapses. Using a cellular α2δ subunit triple-knockout/knockdown model, we demonstrate a failure in presynaptic differentiation evidenced by defective presynaptic calcium channel clustering and calcium influx, smaller presynaptic active zones, and a strongly reduced accumulation of presynaptic vesicle-associated proteins (synapsin and vGLUT). The presynaptic defect is associated with the downscaling of postsynaptic AMPA receptors and the postsynaptic density. The role of α2δ isoforms as synaptic organizers is highly redundant, as each individual α2δ isoform can rescue presynaptic calcium channel trafficking and expression of synaptic proteins. Moreover, α2δ-2 and α2δ-3 with mutated metal ion-dependent adhesion sites can fully rescue presynaptic synapsin expression but only partially calcium channel trafficking, suggesting that the regulatory role of α2δ subunits is independent from its role as a calcium channel subunit. Our findings influence the current view on excitatory synapse formation. First, our study suggests that postsynaptic differentiation is secondary to presynaptic differentiation. Second, the dependence of presynaptic differentiation on α2δ implicates α2δ subunits as potential nucleation points for the organization of synapses. Finally, our results suggest that α2δ subunits act as transsynaptic organizers of glutamatergic synapses, thereby aligning the synaptic active zone with the postsynaptic density.}, author = {Schöpf, Clemens L. and Ablinger, Cornelia and Geisler, Stefanie M. and Stanika, Ruslan I. and Campiglio, Marta and Kaufmann, Walter and Nimmervoll, Benedikt and Schlick, Bettina and Brockhaus, Johannes and Missler, Markus and Shigemoto, Ryuichi and Obermair, Gerald J.}, issn = {1091-6490}, journal = {Proceedings of the National Academy of Sciences of the United States of America}, number = {14}, publisher = {National Academy of Sciences}, title = {{Presynaptic α2δ subunits are key organizers of glutamatergic synapses}}, doi = {10.1073/pnas.1920827118}, volume = {118}, year = {2021}, } @article{9332, abstract = {Lateral root (LR) formation is an example of a plant post-embryonic organogenesis event. LRs are issued from non-dividing cells entering consecutive steps of formative divisions, proliferation and elongation. The chromatin remodeling protein PICKLE (PKL) negatively regulates auxin-mediated LR formation through a mechanism that is not yet known. Here we show that PKL interacts with RETINOBLASTOMA-RELATED 1 (RBR1) to repress the LATERAL ORGAN BOUNDARIES-DOMAIN 16 (LBD16) promoter activity. Since LBD16 function is required for the formative division of LR founder cells, repression mediated by the PKL–RBR1 complex negatively regulates formative division and LR formation. Inhibition of LR formation by PKL–RBR1 is counteracted by auxin, indicating that, in addition to auxin-mediated transcriptional responses, the fine-tuned process of LR formation is also controlled at the chromatin level in an auxin-signaling dependent manner.}, author = {Ötvös, Krisztina and Miskolczi, Pál and Marhavý, Peter and Cruz-Ramírez, Alfredo and Benková, Eva and Robert, Stéphanie and Bakó, László}, issn = {1422-0067}, journal = {International Journal of Molecular Sciences}, number = {8}, publisher = {MDPI}, title = {{Pickle recruits retinoblastoma related 1 to control lateral root formation in arabidopsis}}, doi = {10.3390/ijms22083862}, volume = {22}, year = {2021}, } @article{9333, abstract = {We revise a previous result about the Fröhlich dynamics in the strong coupling limit obtained in Griesemer (Rev Math Phys 29(10):1750030, 2017). In the latter it was shown that the Fröhlich time evolution applied to the initial state φ0⊗ξα, where φ0 is the electron ground state of the Pekar energy functional and ξα the associated coherent state of the phonons, can be approximated by a global phase for times small compared to α2. In the present note we prove that a similar approximation holds for t=O(α2) if one includes a nontrivial effective dynamics for the phonons that is generated by an operator proportional to α−2 and quadratic in creation and annihilation operators. Our result implies that the electron ground state remains close to its initial state for times of order α2, while the phonon fluctuations around the coherent state ξα can be described by a time-dependent Bogoliubov transformation.}, author = {Mitrouskas, David Johannes}, issn = {1573-0530}, journal = {Letters in Mathematical Physics}, publisher = {Springer Nature}, title = {{A note on the Fröhlich dynamics in the strong coupling limit}}, doi = {10.1007/s11005-021-01380-7}, volume = {111}, year = {2021}, } @article{9335, abstract = {Various degenerate diffusion equations exhibit a waiting time phenomenon: depending on the “flatness” of the compactly supported initial datum at the boundary of the support, the support of the solution may not expand for a certain amount of time. We show that this phenomenon is captured by particular Lagrangian discretizations of the porous medium and the thin film equations, and we obtain sufficient criteria for the occurrence of waiting times that are consistent with the known ones for the original PDEs. For the spatially discrete solution, the waiting time phenomenon refers to a deviation of the edge of support from its original position by a quantity comparable to the mesh width, over a mesh-independent time interval. Our proof is based on estimates on the fluid velocity in Lagrangian coordinates. Combining weighted entropy estimates with an iteration technique à la Stampacchia leads to upper bounds on free boundary propagation. Numerical simulations show that the phenomenon is already clearly visible for relatively coarse discretizations.}, author = {Fischer, Julian L and Matthes, Daniel}, issn = {0036-1429}, journal = {SIAM Journal on Numerical Analysis}, number = {1}, pages = {60--87}, publisher = {Society for Industrial and Applied Mathematics}, title = {{The waiting time phenomenon in spatially discretized porous medium and thin film equations}}, doi = {10.1137/19M1300017}, volume = {59}, year = {2021}, } @article{9348, abstract = {We consider the stochastic quantization of a quartic double-well energy functional in the semiclassical regime and derive optimal asymptotics for the exponentially small splitting of the ground state energy. Our result provides an infinite-dimensional version of some sharp tunneling estimates known in finite dimensions for semiclassical Witten Laplacians in degree zero. From a stochastic point of view it proves that the L2 spectral gap of the stochastic one-dimensional Allen-Cahn equation in finite volume satisfies a Kramers-type formula in the limit of vanishing noise. We work with finite-dimensional lattice approximations and establish semiclassical estimates which are uniform in the dimension. Our key estimate shows that the constant separating the two exponentially small eigenvalues from the rest of the spectrum can be taken independently of the dimension.}, author = {Brooks, Morris and Di Gesù, Giacomo}, issn = {1096-0783}, journal = {Journal of Functional Analysis}, number = {3}, publisher = {Elsevier}, title = {{Sharp tunneling estimates for a double-well model in infinite dimension}}, doi = {10.1016/j.jfa.2021.109029}, volume = {281}, year = {2021}, } @article{9350, abstract = {Intercellular adhesion is the key to multicellularity, and its malfunction plays an important role in various developmental and disease-related processes. Although it has been intensively studied by both biologists and physicists, a commonly accepted definition of cell-cell adhesion is still being debated. Cell-cell adhesion has been described at the molecular scale as a function of adhesion receptors controlling binding affinity, at the cellular scale as resistance to detachment forces or modulation of surface tension, and at the tissue scale as a regulator of cellular rearrangements and morphogenesis. In this review, we aim to summarize and discuss recent advances in the molecular, cellular, and theoretical description of cell-cell adhesion, ranging from biomimetic models to the complexity of cells and tissues in an organismal context. In particular, we will focus on cadherin-mediated cell-cell adhesion and the role of adhesion signaling and mechanosensation therein, two processes central for understanding the biological and physical basis of cell-cell adhesion.}, author = {Arslan, Feyza N and Eckert, Julia and Schmidt, Thomas and Heisenberg, Carl-Philipp J}, issn = {1542-0086}, journal = {Biophysical Journal}, pages = {4182--4192}, publisher = {Biophysical Society}, title = {{Holding it together: when cadherin meets cadherin}}, doi = {10.1016/j.bpj.2021.03.025}, volume = {120}, year = {2021}, } @article{9351, abstract = {We consider the many-body quantum evolution of a factorized initial data, in the mean-field regime. We show that fluctuations around the limiting Hartree dynamics satisfy large deviation estimates that are consistent with central limit theorems that have been established in the last years. }, author = {Kirkpatrick, Kay and Rademacher, Simone Anna Elvira and Schlein, Benjamin}, issn = {1424-0637}, journal = {Annales Henri Poincare}, pages = {2595--2618}, publisher = {Springer Nature}, title = {{A large deviation principle in many-body quantum dynamics}}, doi = {10.1007/s00023-021-01044-1}, volume = {22}, year = {2021}, } @article{9352, abstract = {This paper provides an a priori error analysis of a localized orthogonal decomposition method for the numerical stochastic homogenization of a model random diffusion problem. If the uniformly elliptic and bounded random coefficient field of the model problem is stationary and satisfies a quantitative decorrelation assumption in the form of the spectral gap inequality, then the expected $L^2$ error of the method can be estimated, up to logarithmic factors, by $H+(\varepsilon/H)^{d/2}$, $\varepsilon$ being the small correlation length of the random coefficient and $H$ the width of the coarse finite element mesh that determines the spatial resolution. The proof bridges recent results of numerical homogenization and quantitative stochastic homogenization.}, author = {Fischer, Julian L and Gallistl, Dietmar and Peterseim, Dietmar}, issn = {0036-1429}, journal = {SIAM Journal on Numerical Analysis}, number = {2}, pages = {660--674}, publisher = {Society for Industrial and Applied Mathematics}, title = {{A priori error analysis of a numerical stochastic homogenization method}}, doi = {10.1137/19M1308992}, volume = {59}, year = {2021}, } @article{9359, abstract = {We prove that the factorization homologies of a scheme with coefficients in truncated polynomial algebras compute the cohomologies of its generalized configuration spaces. Using Koszul duality between commutative algebras and Lie algebras, we obtain new expressions for the cohomologies of the latter. As a consequence, we obtain a uniform and conceptual approach for treating homological stability, homological densities, and arithmetic densities of generalized configuration spaces. Our results categorify, generalize, and in fact provide a conceptual understanding of the coincidences appearing in the work of Farb--Wolfson--Wood. Our computation of the stable homological densities also yields rational homotopy types, answering a question posed by Vakil--Wood. Our approach hinges on the study of homological stability of cohomological Chevalley complexes, which is of independent interest. }, author = {Ho, Quoc P}, issn = {1364-0380}, journal = {Geometry & Topology}, keywords = {Generalized configuration spaces, homological stability, homological densities, chiral algebras, chiral homology, factorization algebras, Koszul duality, Ran space}, number = {2}, pages = {813--912}, publisher = {Mathematical Sciences Publishers}, title = {{Homological stability and densities of generalized configuration spaces}}, doi = {10.2140/gt.2021.25.813}, volume = {25}, year = {2021}, } @article{9362, abstract = {A central goal in systems neuroscience is to understand the functions performed by neural circuits. Previous top-down models addressed this question by comparing the behaviour of an ideal model circuit, optimised to perform a given function, with neural recordings. However, this requires guessing in advance what function is being performed, which may not be possible for many neural systems. To address this, we propose an inverse reinforcement learning (RL) framework for inferring the function performed by a neural network from data. We assume that the responses of each neuron in a network are optimised so as to drive the network towards ‘rewarded’ states, that are desirable for performing a given function. We then show how one can use inverse RL to infer the reward function optimised by the network from observing its responses. This inferred reward function can be used to predict how the neural network should adapt its dynamics to perform the same function when the external environment or network structure changes. This could lead to theoretical predictions about how neural network dynamics adapt to deal with cell death and/or varying sensory stimulus statistics.}, author = {Chalk, Matthew J and Tkačik, Gašper and Marre, Olivier}, issn = {1932-6203}, journal = {PLoS ONE}, number = {4}, publisher = {Public Library of Science}, title = {{Inferring the function performed by a recurrent neural network}}, doi = {10.1371/journal.pone.0248940}, volume = {16}, year = {2021}, } @article{9363, abstract = {Optogenetics has been harnessed to shed new mechanistic light on current and future therapeutic strategies. This has been to date achieved by the regulation of ion flow and electrical signals in neuronal cells and neural circuits that are known to be affected by disease. In contrast, the optogenetic delivery of trophic biochemical signals, which support cell survival and are implicated in degenerative disorders, has never been demonstrated in an animal model of disease. Here, we reengineered the human and Drosophila melanogaster REarranged during Transfection (hRET and dRET) receptors to be activated by light, creating one-component optogenetic tools termed Opto-hRET and Opto-dRET. Upon blue light stimulation, these receptors robustly induced the MAPK/ERK proliferative signaling pathway in cultured cells. In PINK1B9 flies that exhibit loss of PTEN-induced putative kinase 1 (PINK1), a kinase associated with familial Parkinson’s disease (PD), light activation of Opto-dRET suppressed mitochondrial defects, tissue degeneration and behavioral deficits. In human cells with PINK1 loss-of-function, mitochondrial fragmentation was rescued using Opto-dRET via the PI3K/NF-кB pathway. Our results demonstrate that a light-activated receptor can ameliorate disease hallmarks in a genetic model of PD. The optogenetic delivery of trophic signals is cell type-specific and reversible and thus has the potential to inspire novel strategies towards a spatio-temporal regulation of tissue repair.}, author = {Inglés Prieto, Álvaro and Furthmann, Nikolas and Crossman, Samuel H. and Tichy, Alexandra Madelaine and Hoyer, Nina and Petersen, Meike and Zheden, Vanessa and Bicher, Julia and Gschaider-Reichhart, Eva and György, Attila and Siekhaus, Daria E and Soba, Peter and Winklhofer, Konstanze F. and Janovjak, Harald L}, issn = {1553-7404}, journal = {PLoS genetics}, number = {4}, pages = {e1009479}, publisher = {Public Library of Science}, title = {{Optogenetic delivery of trophic signals in a genetic model of Parkinson's disease}}, doi = {10.1371/journal.pgen.1009479}, volume = {17}, year = {2021}, } @article{9368, abstract = {The quality control system for messenger RNA (mRNA) is fundamental for cellular activities in eukaryotes. To elucidate the molecular mechanism of 3'-Phosphoinositide-Dependent Protein Kinase1 (PDK1), a master regulator that is essential throughout eukaryotic growth and development, we employed a forward genetic approach to screen for suppressors of the loss-of-function T-DNA insertion double mutant pdk1.1 pdk1.2 in Arabidopsis thaliana. Notably, the severe growth attenuation of pdk1.1 pdk1.2 was rescued by sop21 (suppressor of pdk1.1 pdk1.2), which harbours a loss-of-function mutation in PELOTA1 (PEL1). PEL1 is a homologue of mammalian PELOTA and yeast (Saccharomyces cerevisiae) DOM34p, which each form a heterodimeric complex with the GTPase HBS1 (HSP70 SUBFAMILY B SUPPRESSOR1, also called SUPERKILLER PROTEIN7, SKI7), a protein that is responsible for ribosomal rescue and thereby assures the quality and fidelity of mRNA molecules during translation. Genetic analysis further revealed that a dysfunctional PEL1-HBS1 complex failed to degrade the T-DNA-disrupted PDK1 transcripts, which were truncated but functional, and thus rescued the growth and developmental defects of pdk1.1 pdk1.2. Our studies demonstrated the functionality of a homologous PELOTA-HBS1 complex and identified its essential regulatory role in plants, providing insights into the mechanism of mRNA quality control.}, author = {Kong, W and Tan, Shutang and Zhao, Q and Lin, DL and Xu, ZH and Friml, Jiří and Xue, HW}, issn = {1532-2548}, journal = {Plant Physiology}, number = {4}, pages = {2003--2020}, publisher = {American Society of Plant Biologists}, title = {{mRNA surveillance complex PELOTA-HBS1 eegulates phosphoinositide-sependent protein kinase1 and plant growth}}, doi = {10.1093/plphys/kiab199}, volume = {186}, year = {2021}, } @article{9374, abstract = {If there are no constraints on the process of speciation, then the number of species might be expected to match the number of available niches and this number might be indefinitely large. One possible constraint is the opportunity for allopatric divergence. In 1981, Felsenstein used a simple and elegant model to ask if there might also be genetic constraints. He showed that progress towards speciation could be described by the build‐up of linkage disequilibrium among divergently selected loci and between these loci and those contributing to other forms of reproductive isolation. Therefore, speciation is opposed by recombination, because it tends to break down linkage disequilibria. Felsenstein then introduced a crucial distinction between “two‐allele” models, which are subject to this effect, and “one‐allele” models, which are free from the recombination constraint. These fundamentally important insights have been the foundation for both empirical and theoretical studies of speciation ever since.}, author = {Butlin, Roger K. and Servedio, Maria R. and Smadja, Carole M. and Bank, Claudia and Barton, Nicholas H and Flaxman, Samuel M. and Giraud, Tatiana and Hopkins, Robin and Larson, Erica L. and Maan, Martine E. and Meier, Joana and Merrill, Richard and Noor, Mohamed A. F. and Ortiz‐Barrientos, Daniel and Qvarnström, Anna}, issn = {1558-5646}, journal = {Evolution}, keywords = {Genetics, Ecology, Evolution, Behavior and Systematics, General Agricultural and Biological Sciences}, number = {5}, pages = {978--988}, publisher = {Wiley}, title = {{Homage to Felsenstein 1981, or why are there so few/many species?}}, doi = {10.1111/evo.14235}, volume = {75}, year = {2021}, } @article{9375, abstract = {Genetic variation segregates as linked sets of variants, or haplotypes. Haplotypes and linkage are central to genetics and underpin virtually all genetic and selection analysis. And yet, genomic data often lack haplotype information, due to constraints in sequencing technologies. Here we present “haplotagging”, a simple, low-cost linked-read sequencing technique that allows sequencing of hundreds of individuals while retaining linkage information. We apply haplotagging to construct megabase-size haplotypes for over 600 individual butterflies (Heliconius erato and H. melpomene), which form overlapping hybrid zones across an elevational gradient in Ecuador. Haplotagging identifies loci controlling distinctive high- and lowland wing color patterns. Divergent haplotypes are found at the same major loci in both species, while chromosome rearrangements show no parallelism. Remarkably, in both species the geographic clines for the major wing pattern loci are displaced by 18 km, leading to the rise of a novel hybrid morph in the centre of the hybrid zone. We propose that shared warning signalling (Müllerian mimicry) may couple the cline shifts seen in both species, and facilitate the parallel co-emergence of a novel hybrid morph in both co-mimetic species. Our results show the power of efficient haplotyping methods when combined with large-scale sequencing data from natural populations.}, author = {Meier, Joana I. and Salazar, Patricio A. and Kučka, Marek and Davies, Robert William and Dréau, Andreea and Aldás, Ismael and Power, Olivia Box and Nadeau, Nicola J. and Bridle, Jon R. and Rolian, Campbell and Barton, Nicholas H and McMillan, W. Owen and Jiggins, Chris D. and Chan, Yingguang Frank}, issn = {0027-8424}, journal = {Proceedings of the National Academy of Sciences of the United States of America}, number = {25}, publisher = {National Academy of Sciences}, title = {{Haplotype tagging reveals parallel formation of hybrid races in two butterfly species}}, doi = {10.1073/pnas.2015005118}, volume = {118}, year = {2021}, } @article{9376, abstract = {This paper presents a method for designing planar multistable compliant structures. Given a sequence of desired stable states and the corresponding poses of the structure, we identify the topology and geometric realization of a mechanism—consisting of bars and joints—that is able to physically reproduce the desired multistable behavior. In order to solve this problem efficiently, we build on insights from minimally rigid graph theory to identify simple but effective topologies for the mechanism. We then optimize its geometric parameters, such as joint positions and bar lengths, to obtain correct transitions between the given poses. Simultaneously, we ensure adequate stability of each pose based on an effective approximate error metric related to the elastic energy Hessian of the bars in the mechanism. As demonstrated by our results, we obtain functional multistable mechanisms of manageable complexity that can be fabricated using 3D printing. Further, we evaluated the effectiveness of our method on a large number of examples in the simulation and fabricated several physical prototypes.}, author = {Zhang, Ran and Auzinger, Thomas and Bickel, Bernd}, issn = {1557-7368}, journal = {ACM Transactions on Graphics}, keywords = {multistability, mechanism, computational design, rigidity}, number = {5}, publisher = {Association for Computing Machinery}, title = {{Computational design of planar multistable compliant structures}}, doi = {10.1145/3453477}, volume = {40}, year = {2021}, } @article{9379, abstract = {When B cells encounter membrane-bound antigens, the formation and coalescence of B cell antigen receptor (BCR) microclusters amplifies BCR signaling. The ability of B cells to probe the surface of antigen-presenting cells (APCs) and respond to APC-bound antigens requires remodeling of the actin cytoskeleton. Initial BCR signaling stimulates actin-related protein (Arp) 2/3 complex-dependent actin polymerization, which drives B cell spreading as well as the centripetal movement and coalescence of BCR microclusters at the B cell-APC synapse. Sustained actin polymerization depends on concomitant actin filament depolymerization, which enables the recycling of actin monomers and Arp2/3 complexes. Cofilin-mediated severing of actin filaments is a rate-limiting step in the morphological changes that occur during immune synapse formation. Hence, regulators of cofilin activity such as WD repeat-containing protein 1 (Wdr1), LIM domain kinase (LIMK), and coactosin-like 1 (Cotl1) may also be essential for actin-dependent processes in B cells. Wdr1 enhances cofilin-mediated actin disassembly. Conversely, Cotl1 competes with cofilin for binding to actin and LIMK phosphorylates cofilin and prevents it from binding to actin filaments. We now show that Wdr1 and LIMK have distinct roles in BCR-induced assembly of the peripheral actin structures that drive B cell spreading, and that cofilin, Wdr1, and LIMK all contribute to the actin-dependent amplification of BCR signaling at the immune synapse. Depleting Cotl1 had no effect on these processes. Thus, the Wdr1-LIMK-cofilin axis is critical for BCR-induced actin remodeling and for B cell responses to APC-bound antigens.}, author = {Bolger-Munro, Madison and Choi, Kate and Cheung, Faith and Liu, Yi Tian and Dang-Lawson, May and Deretic, Nikola and Keane, Connor and Gold, Michael R.}, issn = {2296-634X}, journal = {Frontiers in Cell and Developmental Biology}, keywords = {B cell, actin, immune synapse, cell spreading, cofilin, WDR1 (AIP1), LIM domain kinase, B cell receptor (BCR)}, publisher = {Frontiers Media}, title = {{The Wdr1-LIMK-Cofilin axis controls B cell antigen receptor-induced actin remodeling and signaling at the immune synapse}}, doi = {10.3389/fcell.2021.649433}, volume = {9}, year = {2021}, } @article{9380, abstract = {Shigella are pathogens originating within the Escherichia lineage but frequently classified as a separate genus. Shigella genomes contain numerous insertion sequences (ISs) that lead to pseudogenisation of affected genes and an increase of non-homologous recombination. Here, we study 414 genomes of E. coli and Shigella strains to assess the contribution of genomic rearrangements to Shigella evolution. We found that Shigella experienced exceptionally high rates of intragenomic rearrangements and had a decreased rate of homologous recombination compared to pathogenic and non-pathogenic E. coli. The high rearrangement rate resulted in independent disruption of syntenic regions and parallel rearrangements in different Shigella lineages. Specifically, we identified two types of chromosomally encoded E3 ubiquitin-protein ligases acquired independently by all Shigella strains that also showed a high level of sequence conservation in the promoter and further in the 5′-intergenic region. In the only available enteroinvasive E. coli (EIEC) strain, which is a pathogenic E. coli with a phenotype intermediate between Shigella and non-pathogenic E. coli, we found a rate of genome rearrangements comparable to those in other E. coli and no functional copies of the two Shigella-specific E3 ubiquitin ligases. These data indicate that the accumulation of ISs influenced many aspects of genome evolution and played an important role in the evolution of intracellular pathogens. Our research demonstrates the power of comparative genomics-based on synteny block composition and an important role of non-coding regions in the evolution of genomic islands.}, author = {Seferbekova, Zaira and Zabelkin, Alexey and Yakovleva, Yulia and Afasizhev, Robert and Dranenko, Natalia O. and Alexeev, Nikita and Gelfand, Mikhail S. and Bochkareva, Olga}, issn = {1664-302X}, journal = {Frontiers in Microbiology}, publisher = {Frontiers}, title = {{High rates of genome rearrangements and pathogenicity of Shigella spp}}, doi = {10.3389/fmicb.2021.628622}, volume = {12}, year = {2021}, } @article{9381, abstract = {A game of rock-paper-scissors is an interesting example of an interaction where none of the pure strategies strictly dominates all others, leading to a cyclic pattern. In this work, we consider an unstable version of rock-paper-scissors dynamics and allow individuals to make behavioural mistakes during the strategy execution. We show that such an assumption can break a cyclic relationship leading to a stable equilibrium emerging with only one strategy surviving. We consider two cases: completely random mistakes when individuals have no bias towards any strategy and a general form of mistakes. Then, we determine conditions for a strategy to dominate all other strategies. However, given that individuals who adopt a dominating strategy are still prone to behavioural mistakes in the observed behaviour, we may still observe extinct strategies. That is, behavioural mistakes in strategy execution stabilise evolutionary dynamics leading to an evolutionary stable and, potentially, mixed co-existence equilibrium.}, author = {Kleshnina, Maria and Streipert, Sabrina S. and Filar, Jerzy A. and Chatterjee, Krishnendu}, issn = {1553-7358}, journal = {PLoS Computational Biology}, number = {4}, publisher = {Public Library of Science}, title = {{Mistakes can stabilise the dynamics of rock-paper-scissors games}}, doi = {10.1371/journal.pcbi.1008523}, volume = {17}, year = {2021}, }