@inbook{8092,
  abstract     = {Image translation refers to the task of mapping images from a visual domain to another. Given two unpaired collections of images, we aim to learn a mapping between the corpus-level style of each collection, while preserving semantic content shared across the two domains. We introduce xgan, a dual adversarial auto-encoder, which captures a shared representation of the common domain semantic content in an unsupervised way, while jointly learning the domain-to-domain image translations in both directions. We exploit ideas from the domain adaptation literature and define a semantic consistency loss which encourages the learned embedding to preserve semantics shared across domains. We report promising qualitative results for the task of face-to-cartoon translation. The cartoon dataset we collected for this purpose, “CartoonSet”, is also publicly available as a new benchmark for semantic style transfer at https://google.github.io/cartoonset/index.html.},
  author       = {Royer, Amélie and Bousmalis, Konstantinos and Gouws, Stephan and Bertsch, Fred and Mosseri, Inbar and Cole, Forrester and Murphy, Kevin},
  booktitle    = {Domain Adaptation for Visual Understanding},
  editor       = {Singh, Richa and Vatsa, Mayank and Patel, Vishal M. and Ratha, Nalini},
  isbn         = {9783030306717},
  pages        = {33--49},
  publisher    = {Springer Nature},
  title        = {{XGAN: Unsupervised image-to-image translation for many-to-many mappings}},
  doi          = {10.1007/978-3-030-30671-7_3},
  year         = {2020},
}

@article{8093,
  abstract     = {Background: The activation of the EGFR/Ras-signalling pathway in tumour cells induces a distinct chemokine repertoire, which in turn modulates the tumour microenvironment.
Methods: The effects of EGFR/Ras on the expression and translation of CCL20 were analysed in a large set of epithelial cancer cell lines and tumour tissues by RT-qPCR and ELISA in vitro. CCL20 production was verified by immunohistochemistry in different tumour tissues and correlated with clinical data. The effects of CCL20 on endothelial cell migration and tumour-associated vascularisation were comprehensively analysed with chemotaxis assays in vitro and in CCR6-deficient mice in vivo.
Results: Tumours facilitate progression by the EGFR/Ras-induced production of CCL20. Expression of the chemokine CCL20 in tumours correlates with advanced tumour stage, increased lymph node metastasis and decreased survival in patients. Microvascular endothelial cells abundantly express the specific CCL20 receptor CCR6. CCR6 signalling in endothelial cells induces angiogenesis. CCR6-deficient mice show significantly decreased tumour growth and tumour-associated vascularisation. The observed phenotype is dependent on CCR6 deficiency in stromal cells but not within the immune system.
Conclusion: We propose that the chemokine axis CCL20–CCR6 represents a novel and promising target to interfere with the tumour microenvironment, and opens an innovative multimodal strategy for cancer therapy.},
  author       = {Hippe, Andreas and Braun, Stephan Alexander and Oláh, Péter and Gerber, Peter Arne and Schorr, Anne and Seeliger, Stephan and Holtz, Stephanie and Jannasch, Katharina and Pivarcsi, Andor and Buhren, Bettina and Schrumpf, Holger and Kislat, Andreas and Bünemann, Erich and Steinhoff, Martin and Fischer, Jens and Lira, Sérgio A. and Boukamp, Petra and Hevezi, Peter and Stoecklein, Nikolas Hendrik and Hoffmann, Thomas and Alves, Frauke and Sleeman, Jonathan and Bauer, Thomas and Klufa, Jörg and Amberg, Nicole and Sibilia, Maria and Zlotnik, Albert and Müller-Homey, Anja and Homey, Bernhard},
  issn         = {1532-1827},
  journal      = {British Journal of Cancer},
  pages        = {942--954},
  publisher    = {Springer Nature},
  title        = {{EGFR/Ras-induced CCL20 production modulates the tumour microenvironment}},
  doi          = {10.1038/s41416-020-0943-2},
  volume       = {123},
  year         = {2020},
}

@misc{8097,
  abstract     = {Antibiotics that interfere with translation, when combined, interact in diverse and difficult-to-predict ways. Here, we explain these interactions by "translation bottlenecks": points in the translation cycle where antibiotics block ribosomal progression. To elucidate the underlying mechanisms of drug interactions between translation inhibitors, we generate translation bottlenecks genetically using inducible control of translation factors that regulate well-defined translation cycle steps. These perturbations accurately mimic antibiotic action and drug interactions, supporting that the interplay of different translation bottlenecks causes these interactions. We further show that growth laws, combined with drug uptake and binding kinetics, enable the direct prediction of a large fraction of observed interactions, yet fail to predict suppression. However, varying two translation bottlenecks simultaneously supports that dense traffic of ribosomes and competition for translation factors account for the previously unexplained suppression. These results highlight the importance of "continuous epistasis" in bacterial physiology.},
  author       = {Kavcic, Bor},
  keywords     = {Escherichia coli, antibiotic combinations, translation, growth laws, drug interactions, bacterial physiology, translation inhibitors},
  publisher    = {Institute of Science and Technology Austria},
  title        = {{Analysis scripts and research data for the paper "Mechanisms of drug interactions between translation-inhibiting antibiotics"}},
  doi          = {10.15479/AT:ISTA:8097},
  year         = {2020},
}

@article{8099,
  abstract     = {Sewall Wright developed FST for describing population differentiation and it has since been extended to many novel applications, including the detection of homomorphic sex chromosomes. However, there has been confusion regarding the expected estimate of FST for a fixed difference between the X‐ and Y‐chromosome when comparing males and females. Here, we attempt to resolve this confusion by contrasting two common FST estimators and explain why they yield different estimates when applied to the case of sex chromosomes. We show that this difference is true for many allele frequencies, but the situation characterized by fixed differences between the X‐ and Y‐chromosome is among the most extreme. To avoid additional confusion, we recommend that all authors using FST clearly state which estimator of FST their work uses.},
  author       = {Gammerdinger, William J and Toups, Melissa A and Vicoso, Beatriz},
  issn         = {1755-0998},
  journal      = {Molecular Ecology Resources},
  number       = {6},
  pages        = {1517--1525},
  publisher    = {Wiley},
  title        = {{Disagreement in FST estimators: A case study from  sex chromosomes}},
  doi          = {10.1111/1755-0998.13210},
  volume       = {20},
  year         = {2020},
}

@article{8101,
  abstract     = {By rigorously accounting for mesoscale spatial correlations in donor/acceptor surface properties, we develop a scale-spanning model for same-material tribocharging. We find that mesoscale correlations affect not only the magnitude of charge transfer but also the fluctuations—suppressing otherwise overwhelming charge-transfer variability that is not observed experimentally. We furthermore propose a generic theoretical mechanism by which the mesoscale features might emerge, which is qualitatively consistent with other proposals in the literature.},
  author       = {Grosjean, Galien M and Wald, Sebastian and Sobarzo Ponce, Juan Carlos A and Waitukaitis, Scott R},
  issn         = {2475-9953},
  journal      = {Physical Review Materials},
  keywords     = {electric charge, tribocharging, soft matter, granular materials, polymers},
  number       = {8},
  publisher    = {American Physical Society},
  title        = {{Quantitatively consistent scale-spanning model for same-material tribocharging}},
  doi          = {10.1103/PhysRevMaterials.4.082602},
  volume       = {4},
  year         = {2020},
}

@article{8105,
  abstract     = {Physical and biological systems often exhibit intermittent dynamics with bursts or avalanches (active states) characterized by power-law size and duration distributions. These emergent features are typical of systems at the critical point of continuous phase transitions, and have led to the hypothesis that such systems may self-organize at criticality, i.e. without any fine tuning of parameters. Since the introduction of the Bak-Tang-Wiesenfeld (BTW) model, the paradigm of self-organized criticality (SOC) has been very fruitful for the analysis of emergent collective behaviors in a number of systems, including the brain. Although considerable effort has been devoted in identifying and modeling scaling features of burst and avalanche statistics, dynamical aspects related to the temporal organization of bursts remain often poorly understood or controversial. Of crucial importance to understand the mechanisms responsible for emergent behaviors is the relationship between active and quiet periods, and the nature of the correlations. Here we investigate the dynamics of active (θ-bursts) and quiet states (δ-bursts) in brain activity during the sleep-wake cycle. We show the duality of power-law (θ, active phase) and exponential-like (δ, quiescent phase) duration distributions, typical of SOC, jointly emerge with power-law temporal correlations and anti-correlated coupling between active and quiet states. Importantly, we demonstrate that such temporal organization shares important similarities with earthquake dynamics, and propose that specific power-law correlations and coupling between active and quiet states are distinctive characteristics of a class of systems with self-organization at criticality.},
  author       = {Lombardi, Fabrizio and Wang, Jilin W.J.L. and Zhang, Xiyun and Ivanov, Plamen Ch},
  issn         = {2100-014X},
  journal      = {EPJ Web of Conferences},
  publisher    = {EDP Sciences},
  title        = {{Power-law correlations and coupling of active and quiet states underlie a class of complex systems with self-organization at criticality}},
  doi          = {10.1051/epjconf/202023000005},
  volume       = {230},
  year         = {2020},
}

@article{8112,
  author       = {Barton, Nicholas H},
  issn         = {1471-2970},
  journal      = {Philosophical Transactions of the Royal Society. Series B: Biological Sciences},
  number       = {1806},
  publisher    = {The Royal Society},
  title        = {{On the completion of speciation}},
  doi          = {10.1098/rstb.2019.0530},
  volume       = {375},
  year         = {2020},
}

@article{8126,
  abstract     = {Cortical areas comprise multiple types of inhibitory interneurons with stereotypical connectivity motifs, but their combined effect on postsynaptic dynamics has been largely unexplored. Here, we analyse the response of a single postsynaptic model neuron receiving tuned excitatory connections alongside inhibition from two plastic populations. Depending on the inhibitory plasticity rule, synapses remain unspecific (flat), become anti-correlated to, or mirror excitatory synapses. Crucially, the neuron’s receptive field, i.e., its response to presynaptic stimuli, depends on the modulatory state of inhibition. When both inhibitory populations are active, inhibition balances excitation, resulting in uncorrelated postsynaptic responses regardless of the inhibitory tuning profiles. Modulating the activity of a given inhibitory population produces strong correlations to either preferred or non-preferred inputs, in line with recent experimental findings showing dramatic context-dependent changes of neurons’ receptive fields. We thus confirm that a neuron’s receptive field doesn’t follow directly from the weight profiles of its presynaptic afferents.},
  author       = {Agnes, Everton J. and Luppi, Andrea I. and Vogels, Tim P},
  issn         = {1529-2401},
  journal      = {The Journal of Neuroscience},
  number       = {50},
  pages        = {9634--9649},
  publisher    = {Society for Neuroscience},
  title        = {{Complementary inhibitory weight profiles emerge from plasticity and allow attentional switching of receptive fields}},
  doi          = {10.1523/JNEUROSCI.0276-20.2020},
  volume       = {40},
  year         = {2020},
}

@article{8127,
  abstract     = {Mechanistic modeling in neuroscience aims to explain observed phenomena in terms of underlying causes. However, determining which model parameters agree with complex and stochastic neural data presents a significant challenge. We address this challenge with a machine learning tool which uses deep neural density estimators—trained using model simulations—to carry out Bayesian inference and retrieve the full space of parameters compatible with raw data or selected data features. Our method is scalable in parameters and data features and can rapidly analyze new data after initial training. We demonstrate the power and flexibility of our approach on receptive fields, ion channels, and Hodgkin–Huxley models. We also characterize the space of circuit configurations giving rise to rhythmic activity in the crustacean stomatogastric ganglion, and use these results to derive hypotheses for underlying compensation mechanisms. Our approach will help close the gap between data-driven and theory-driven models of neural dynamics.},
  author       = {Gonçalves, Pedro J. and Lueckmann, Jan-Matthis and Deistler, Michael and Nonnenmacher, Marcel and Öcal, Kaan and Bassetto, Giacomo and Chintaluri, Chaitanya and Podlaski, William F. and Haddad, Sara A. and Vogels, Tim P and Greenberg, David S. and Macke, Jakob H.},
  issn         = {2050-084X},
  journal      = {eLife},
  publisher    = {eLife Sciences Publications},
  title        = {{Training deep neural density estimators to identify mechanistic models of neural dynamics}},
  doi          = {10.7554/eLife.56261},
  volume       = {9},
  year         = {2020},
}

@article{8130,
  abstract     = {We study the dynamics of a system of N interacting bosons in a disc-shaped trap, which is realised by an external potential that confines the bosons in one spatial dimension to an interval of length of order ε. The interaction is non-negative and scaled in such a way that its scattering length is of order ε/N, while its range is proportional to (ε/N)β with scaling parameter β∈(0,1]. We consider the simultaneous limit (N,ε)→(∞,0) and assume that the system initially exhibits Bose–Einstein condensation. We prove that condensation is preserved by the N-body dynamics, where the time-evolved condensate wave function is the solution of a two-dimensional non-linear equation. The strength of the non-linearity depends on the scaling parameter β. For β∈(0,1), we obtain a cubic defocusing non-linear Schrödinger equation, while the choice β=1 yields a Gross–Pitaevskii equation featuring the scattering length of the interaction. In both cases, the coupling parameter depends on the confining potential.},
  author       = {Bossmann, Lea},
  issn         = {1432-0673},
  journal      = {Archive for Rational Mechanics and Analysis},
  number       = {11},
  pages        = {541--606},
  publisher    = {Springer Nature},
  title        = {{Derivation of the 2d Gross–Pitaevskii equation for strongly confined 3d Bosons}},
  doi          = {10.1007/s00205-020-01548-w},
  volume       = {238},
  year         = {2020},
}

@article{8131,
  abstract     = {The possibility to generate construct valid animal models enabled the development and testing of therapeutic strategies targeting the core features of autism spectrum disorders (ASDs). At the same time, these studies highlighted the necessity of identifying sensitive developmental time windows for successful therapeutic interventions. Animal and human studies also uncovered the possibility to stratify the variety of ASDs in molecularly distinct subgroups, potentially facilitating effective treatment design. Here, we focus on the molecular pathways emerging as commonly affected by mutations in diverse ASD-risk genes, on their role during critical windows of brain development and the potential treatments targeting these biological processes.},
  author       = {Basilico, Bernadette and Morandell, Jasmin and Novarino, Gaia},
  issn         = {18790380},
  journal      = {Current Opinion in Genetics and Development},
  number       = {12},
  pages        = {126--137},
  publisher    = {Elsevier},
  title        = {{Molecular mechanisms for targeted ASD treatments}},
  doi          = {10.1016/j.gde.2020.06.004},
  volume       = {65},
  year         = {2020},
}

@article{8132,
  abstract     = {The WAVE regulatory complex (WRC) is crucial for assembly of the peripheral branched actin network constituting one of the main drivers of eukaryotic cell migration. Here, we uncover an essential role of the hematopoietic-specific WRC component HEM1 for immune cell development. Germline-encoded HEM1 deficiency underlies an inborn error of immunity with systemic autoimmunity, at cellular level marked by WRC destabilization, reduced filamentous actin, and failure to assemble lamellipodia. Hem1−/− mice display systemic autoimmunity, phenocopying the human disease. In the absence of Hem1, B cells become deprived of extracellular stimuli necessary to maintain the strength of B cell receptor signaling at a level permissive for survival of non-autoreactive B cells. This shifts the balance of B cell fate choices toward autoreactive B cells and thus autoimmunity.},
  author       = {Salzer, Elisabeth and Zoghi, Samaneh and Kiss, Máté G. and Kage, Frieda and Rashkova, Christina and Stahnke, Stephanie and Haimel, Matthias and Platzer, René and Caldera, Michael and Ardy, Rico Chandra and Hoeger, Birgit and Block, Jana and Medgyesi, David and Sin, Celine and Shahkarami, Sepideh and Kain, Renate and Ziaee, Vahid and Hammerl, Peter and Bock, Christoph and Menche, Jörg and Dupré, Loïc and Huppa, Johannes B. and Sixt, Michael K and Lomakin, Alexis and Rottner, Klemens and Binder, Christoph J. and Stradal, Theresia E.B. and Rezaei, Nima and Boztug, Kaan},
  issn         = {24709468},
  journal      = {Science Immunology},
  number       = {49},
  publisher    = {AAAS},
  title        = {{The cytoskeletal regulator HEM1 governs B cell development and prevents autoimmunity}},
  doi          = {10.1126/sciimmunol.abc3979},
  volume       = {5},
  year         = {2020},
}

@article{8133,
  abstract     = {The molecular factors which control circulating levels of inflammatory proteins are not well understood. Furthermore, association studies between molecular probes and human traits are often performed by linear model-based methods which may fail to account for complex structure and interrelationships within molecular datasets.In this study, we perform genome- and epigenome-wide association studies (GWAS/EWAS) on the levels of 70 plasma-derived inflammatory protein biomarkers in healthy older adults (Lothian Birth Cohort 1936; n = 876; Olink® inflammation panel). We employ a Bayesian framework (BayesR+) which can account for issues pertaining to data structure and unknown confounding variables (with sensitivity analyses using ordinary least squares- (OLS) and mixed model-based approaches). We identified 13 SNPs associated with 13 proteins (n = 1 SNP each) concordant across OLS and Bayesian methods. We identified 3 CpG sites spread across 3 proteins (n = 1 CpG each) that were concordant across OLS, mixed-model and Bayesian analyses. Tagged genetic variants accounted for up to 45% of variance in protein levels (for MCP2, 36% of variance alone attributable to 1 polymorphism). Methylation data accounted for up to 46% of variation in protein levels (for CXCL10). Up to 66% of variation in protein levels (for VEGFA) was explained using genetic and epigenetic data combined. We demonstrated putative causal relationships between CD6 and IL18R1 with inflammatory bowel disease and between IL12B and Crohn’s disease. Our data may aid understanding of the molecular regulation of the circulating inflammatory proteome as well as causal relationships between inflammatory mediators and disease.},
  author       = {Hillary, Robert F. and Trejo-Banos, Daniel and Kousathanas, Athanasios and Mccartney, Daniel L. and Harris, Sarah E. and Stevenson, Anna J. and Patxot, Marion and Ojavee, Sven Erik and Zhang, Qian and Liewald, David C. and Ritchie, Craig W. and Evans, Kathryn L. and Tucker-Drob, Elliot M. and Wray, Naomi R. and Mcrae, Allan F. and Visscher, Peter M. and Deary, Ian J. and Robinson, Matthew Richard and Marioni, Riccardo E.},
  issn         = {1756994X},
  journal      = {Genome Medicine},
  number       = {1},
  publisher    = {Springer Nature},
  title        = {{Multi-method genome- and epigenome-wide studies of inflammatory protein levels in healthy older adults}},
  doi          = {10.1186/s13073-020-00754-1},
  volume       = {12},
  year         = {2020},
}

@article{8134,
  abstract     = {We prove an upper bound on the free energy of a two-dimensional homogeneous Bose gas in the thermodynamic limit. We show that for a2ρ ≪ 1 and βρ ≳ 1, the free energy per unit volume differs from the one of the non-interacting system by at most 4πρ2|lna2ρ|−1(2−[1−βc/β]2+) to leading order, where a is the scattering length of the two-body interaction potential, ρ is the density, β is the inverse temperature, and βc is the inverse Berezinskii–Kosterlitz–Thouless critical temperature for superfluidity. In combination with the corresponding matching lower bound proved by Deuchert et al. [Forum Math. Sigma 8, e20 (2020)], this shows equality in the asymptotic expansion.},
  author       = {Mayer, Simon and Seiringer, Robert},
  issn         = {00222488},
  journal      = {Journal of Mathematical Physics},
  number       = {6},
  publisher    = {AIP Publishing},
  title        = {{The free energy of the two-dimensional dilute Bose gas. II. Upper bound}},
  doi          = {10.1063/5.0005950},
  volume       = {61},
  year         = {2020},
}

@inproceedings{8135,
  abstract     = {Discrete Morse theory has recently lead to new developments in the theory of random geometric complexes. This article surveys the methods and results obtained with this new approach, and discusses some of its shortcomings. It uses simulations to illustrate the results and to form conjectures, getting numerical estimates for combinatorial, topological, and geometric properties of weighted and unweighted Delaunay mosaics, their dual Voronoi tessellations, and the Alpha and Wrap complexes contained in the mosaics.},
  author       = {Edelsbrunner, Herbert and Nikitenko, Anton and Ölsböck, Katharina and Synak, Peter},
  booktitle    = {Topological Data Analysis},
  isbn         = {9783030434076},
  issn         = {21978549},
  pages        = {181--218},
  publisher    = {Springer Nature},
  title        = {{Radius functions on Poisson–Delaunay mosaics and related complexes experimentally}},
  doi          = {10.1007/978-3-030-43408-3_8},
  volume       = {15},
  year         = {2020},
}

@article{8138,
  abstract     = {Directional transport of the phytohormone auxin is a versatile, plant-specific mechanism regulating many aspects of plant development. The recently identified plant hormones, strigolactones (SLs), are implicated in many plant traits; among others, they modify the phenotypic output of PIN-FORMED (PIN) auxin transporters for fine-tuning of growth and developmental responses. Here, we show in pea and Arabidopsis that SLs target processes dependent on the canalization of auxin flow, which involves auxin feedback on PIN subcellular distribution. D14 receptor- and MAX2 F-box-mediated SL signaling inhibits the formation of auxin-conducting channels after wounding or from artificial auxin sources, during vasculature de novo formation and regeneration. At the cellular level, SLs interfere with auxin effects on PIN polar targeting, constitutive PIN trafficking as well as clathrin-mediated endocytosis. Our results identify a non-transcriptional mechanism of SL action, uncoupling auxin feedback on PIN polarity and trafficking, thereby regulating vascular tissue formation and regeneration.},
  author       = {Zhang, J and Mazur, E and Balla, J and Gallei, Michelle C and Kalousek, P and Medveďová, Z and Li, Y and Wang, Y and Prat, Tomas and Vasileva, Mina K and Reinöhl, V and Procházka, S and Halouzka, R and Tarkowski, P and Luschnig, C and Brewer, PB and Friml, Jiří},
  issn         = {2041-1723},
  journal      = {Nature Communications},
  number       = {1},
  pages        = {3508},
  publisher    = {Springer Nature},
  title        = {{Strigolactones inhibit auxin feedback on PIN-dependent auxin transport canalization}},
  doi          = {10.1038/s41467-020-17252-y},
  volume       = {11},
  year         = {2020},
}

@article{8139,
  abstract     = {Clathrin-mediated endocytosis (CME) is a crucial cellular process implicated in many aspects of plant growth, development, intra- and inter-cellular signaling, nutrient uptake and pathogen defense. Despite these significant roles, little is known about the precise molecular details of how it functions in planta. In order to facilitate the direct quantitative study of plant CME, here we review current routinely used methods and present refined, standardized quantitative imaging protocols which allow the detailed characterization of CME at multiple scales in plant tissues. These include: (i) an efficient electron microscopy protocol for the imaging of Arabidopsis CME vesicles in situ, thus providing a method for the detailed characterization of the ultra-structure of clathrin-coated vesicles; (ii) a detailed protocol and analysis for quantitative live-cell fluorescence microscopy to precisely examine the temporal interplay of endocytosis components during single CME events; (iii) a semi-automated analysis to allow the quantitative characterization of global internalization of cargos in whole plant tissues; and (iv) an overview and validation of useful genetic and pharmacological tools to interrogate the molecular mechanisms and function of CME in intact plant samples.},
  author       = {Johnson, Alexander J and Gnyliukh, Nataliia and Kaufmann, Walter and Narasimhan, Madhumitha and Vert, G and Bednarek, SY and Friml, Jiří},
  issn         = {1477-9137},
  journal      = {Journal of Cell Science},
  number       = {15},
  publisher    = {The Company of Biologists},
  title        = {{Experimental toolbox for quantitative evaluation of clathrin-mediated endocytosis in the plant model Arabidopsis}},
  doi          = {10.1242/jcs.248062},
  volume       = {133},
  year         = {2020},
}

@article{8142,
  abstract     = {Cell production and differentiation for the acquisition of specific functions are key features of living systems. The dynamic network of cellular microtubules provides the necessary platform to accommodate processes associated with the transition of cells through the individual phases of cytogenesis. Here, we show that the plant hormone cytokinin fine‐tunes the activity of the microtubular cytoskeleton during cell differentiation and counteracts microtubular rearrangements driven by the hormone auxin. The endogenous upward gradient of cytokinin activity along the longitudinal growth axis in Arabidopsis thaliana roots correlates with robust rearrangements of the microtubule cytoskeleton in epidermal cells progressing from the proliferative to the differentiation stage. Controlled increases in cytokinin activity result in premature re‐organization of the microtubule network from transversal to an oblique disposition in cells prior to their differentiation, whereas attenuated hormone perception delays cytoskeleton conversion into a configuration typical for differentiated cells. Intriguingly, cytokinin can interfere with microtubules also in animal cells, such as leukocytes, suggesting that a cytokinin‐sensitive control pathway for the microtubular cytoskeleton may be at least partially conserved between plant and animal cells.},
  author       = {Montesinos López, Juan C and Abuzeineh, A and Kopf, Aglaja and Juanes Garcia, Alba and Ötvös, Krisztina and Petrášek, J and Sixt, Michael K and Benková, Eva},
  issn         = {1460-2075},
  journal      = {The Embo Journal},
  number       = {17},
  publisher    = {Embo Press},
  title        = {{Phytohormone cytokinin guides microtubule dynamics during cell progression from proliferative to differentiated stage}},
  doi          = {10.15252/embj.2019104238},
  volume       = {39},
  year         = {2020},
}

@techreport{8151,
  abstract     = {The main idea behind the Core Project is to teach first year students at IST scientific communication skills and let them practice by presenting their research within an interdisciplinary environment. Over the course of the first semester, students participated in seminars, where they shared their results with the colleagues from other fields and took part in discussions on relevant subjects. The main focus during this sessions was on delivering the information in a simplified and comprehensible way, going into the very basics of a subject if necessary. At the end, the students were asked to present their research in the written form to exercise their writing skills. The reports were gathered in this document. All of them were reviewed by the  teaching assistants and write-ups illustrating unique stylistic features and, in general, an outstanding level of writing skills, were honorably mentioned in the section "Selected Reports".},
  author       = {Maslov, Mikhail and Kondrashov, Fyodor and Artner, Christina and Hennessey-Wesen, Mike and Kavcic, Bor and Machnik, Nick N and Satapathy, Roshan K and Tomanek, Isabella},
  pages        = {425},
  publisher    = {IST Austria},
  title        = {{Core Project Proceedings}},
  year         = {2020},
}

@phdthesis{8155,
  abstract     = {In the thesis we focus on the interplay of the biophysics and evolution of gene regulation. We start by addressing how the type of prokaryotic gene regulation – activation and repression – affects spurious binding to DNA, also known as
transcriptional crosstalk. We propose that regulatory interference caused by excess regulatory proteins in the dense cellular medium – global crosstalk – could be a factor in determining which type of gene regulatory network is evolutionarily preferred. Next,we use a normative approach in eukaryotic gene regulation to describe minimal
non-equilibrium enhancer models that optimize so-called regulatory phenotypes. We find a class of models that differ from standard thermodynamic equilibrium models by a single parameter that notably increases the regulatory performance. Next chapter addresses the question of genotype-phenotype-fitness maps of higher dimensional phenotypes. We show that our biophysically realistic approach allows us to understand how the mechanisms of promoter function constrain genotypephenotype maps, and how they affect the evolutionary trajectories of promoters.
In the last chapter we ask whether the intrinsic instability of gene duplication and amplification provides a generic alternative to canonical gene regulation. Using mathematical modeling, we show that amplifications can tune gene expression in many environments, including those where transcription factor-based schemes are
hard to evolve or maintain. },
  author       = {Grah, Rok},
  issn         = {2663-337X},
  pages        = {310},
  publisher    = {Institute of Science and Technology Austria},
  title        = {{Gene regulation across scales – how biophysical constraints shape evolution}},
  doi          = {10.15479/AT:ISTA:8155},
  year         = {2020},
}