@article{12188, abstract = {Molecular mechanisms enabling the switching and maintenance of epigenetic states are not fully understood. Distinct histone modifications are often associated with ON/OFF epigenetic states, but how these states are stably maintained through DNA replication, yet in certain situations switch from one to another remains unclear. Here, we address this problem through identification of Arabidopsis INCURVATA11 (ICU11) as a Polycomb Repressive Complex 2 accessory protein. ICU11 robustly immunoprecipitated in vivo with PRC2 core components and the accessory proteins, EMBRYONIC FLOWER 1 (EMF1), LIKE HETEROCHROMATIN PROTEIN1 (LHP1), and TELOMERE_REPEAT_BINDING FACTORS (TRBs). ICU11 encodes a 2-oxoglutarate-dependent dioxygenase, an activity associated with histone demethylation in other organisms, and mutant plants show defects in multiple aspects of the Arabidopsis epigenome. To investigate its primary molecular function we identified the Arabidopsis FLOWERING LOCUS C (FLC) as a direct target and found icu11 disrupted the cold-induced, Polycomb-mediated silencing underlying vernalization. icu11 prevented reduction in H3K36me3 levels normally seen during the early cold phase, supporting a role for ICU11 in H3K36me3 demethylation. This was coincident with an attenuation of H3K27me3 at the internal nucleation site in FLC, and reduction in H3K27me3 levels across the body of the gene after plants were returned to the warm. Thus, ICU11 is required for the cold-induced epigenetic switching between the mutually exclusive chromatin states at FLC, from the active H3K36me3 state to the silenced H3K27me3 state. These data support the importance of physical coupling of histone modification activities to promote epigenetic switching between opposing chromatin states.}, author = {Bloomer, Rebecca H. and Hutchison, Claire E. and Bäurle, Isabel and Walker, James and Fang, Xiaofeng and Perera, Pumi and Velanis, Christos N. and Gümüs, Serin and Spanos, Christos and Rappsilber, Juri and Feng, Xiaoqi and Goodrich, Justin and Dean, Caroline}, issn = {0027-8424}, journal = {Proceedings of the National Academy of Sciences}, keywords = {Multidisciplinary}, number = {28}, pages = {16660--16666}, publisher = {Proceedings of the National Academy of Sciences}, title = {{The Arabidopsis epigenetic regulator ICU11 as an accessory protein of polycomb repressive complex 2}}, doi = {10.1073/pnas.1920621117}, volume = {117}, year = {2020}, } @article{12189, abstract = {Meiotic crossovers (COs) are important for reshuffling genetic information between homologous chromosomes and they are essential for their correct segregation. COs are unevenly distributed along chromosomes and the underlying mechanisms controlling CO localization are not well understood. We previously showed that meiotic COs are mis-localized in the absence of AXR1, an enzyme involved in the neddylation/rubylation protein modification pathway in Arabidopsis thaliana. Here, we report that in axr1-/-, male meiocytes show a strong defect in chromosome pairing whereas the formation of the telomere bouquet is not affected. COs are also redistributed towards subtelomeric chromosomal ends where they frequently form clusters, in contrast to large central regions depleted in recombination. The CO suppressed regions correlate with DNA hypermethylation of transposable elements (TEs) in the CHH context in axr1-/- meiocytes. Through examining somatic methylomes, we found axr1-/- affects DNA methylation in a plant, causing hypermethylation in all sequence contexts (CG, CHG and CHH) in TEs. Impairment of the main pathways involved in DNA methylation is epistatic over axr1-/- for DNA methylation in somatic cells but does not restore regular chromosome segregation during meiosis. Collectively, our findings reveal that the neddylation pathway not only regulates hormonal perception and CO distribution but is also, directly or indirectly, a major limiting pathway of TE DNA methylation in somatic cells.}, author = {Christophorou, Nicolas and She, Wenjing and Long, Jincheng and Hurel, Aurélie and Beaubiat, Sébastien and Idir, Yassir and Tagliaro-Jahns, Marina and Chambon, Aurélie and Solier, Victor and Vezon, Daniel and Grelon, Mathilde and Feng, Xiaoqi and Bouché, Nicolas and Mézard, Christine}, issn = {1553-7404}, journal = {PLOS Genetics}, keywords = {Cancer Research, Genetics (clinical), Genetics, Molecular Biology, Ecology, Evolution, Behavior and Systematics}, number = {6}, publisher = {Public Library of Science (PLoS)}, title = {{AXR1 affects DNA methylation independently of its role in regulating meiotic crossover localization}}, doi = {10.1371/journal.pgen.1008894}, volume = {16}, year = {2020}, } @misc{9706, abstract = {Additional file 2: Supplementary Tables. The association of pre-adjusted protein levels with biological and technical covariates. Protein levels were adjusted for age, sex, array plate and four genetic principal components (population structure) prior to analyses. Significant associations are emboldened. (Table S1). pQTLs associated with inflammatory biomarker levels from Bayesian penalised regression model (Posterior Inclusion Probability > 95%). (Table S2). All pQTLs associated with inflammatory biomarker levels from ordinary least squares regression model (P < 7.14 × 10− 10). (Table S3). Summary of lambda values relating to ordinary least squares GWAS and EWAS performed on inflammatory protein levels (n = 70) in Lothian Birth Cohort 1936 study. (Table S4). Conditionally significant pQTLs associated with inflammatory biomarker levels from ordinary least squares regression model (P < 7.14 × 10− 10). (Table S5). Comparison of variance explained by ordinary least squares and Bayesian penalised regression models for concordantly identified SNPs. (Table S6). Estimate of heritability for blood protein levels as well as proportion of variance explained attributable to different prior mixtures. (Table S7). Comparison of heritability estimates from Ahsan et al. (maximum likelihood) and Hillary et al. (Bayesian penalised regression). (Table S8). List of concordant SNPs identified by linear model and Bayesian penalised regression and whether they have been previously identified as eQTLs. (Table S9). Bayesian tests of colocalisation for cis pQTLs and cis eQTLs. (Table S10). Sherlock algorithm: Genes whose expression are putatively associated with circulating inflammatory proteins that harbour pQTLs. (Table S11). CpGs associated with inflammatory protein biomarkers as identified by Bayesian model (Bayesian model; Posterior Inclusion Probability > 95%). (Table S12). CpGs associated with inflammatory protein biomarkers as identified by linear model (limma) at P < 5.14 × 10− 10. (Table S13). CpGs associated with inflammatory protein biomarkers as identified by mixed linear model (OSCA) at P < 5.14 × 10− 10. (Table S14). Estimate of variance explained for blood protein levels by DNA methylation as well as proportion of explained attributable to different prior mixtures - BayesR+. (Table S15). Comparison of variance in protein levels explained by genome-wide DNA methylation data by mixed linear model (OSCA) and Bayesian penalised regression model (BayesR+). (Table S16). Variance in circulating inflammatory protein biomarker levels explained by common genetic and methylation data (joint and conditional estimates from BayesR+). Ordered by combined variance explained by genetic and epigenetic data - smallest to largest. Significant results from t-tests comparing distributions for variance explained by methylation or genetics alone versus combined estimate are emboldened. (Table S17). Genetic and epigenetic factors identified by BayesR+ when conditioning on all SNPs and CpGs together. (Table S18). Mendelian Randomisation analyses to assess whether proteins with concordantly identified genetic signals are causally associated with Alzheimer’s disease risk. (Table S19).}, 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. }, publisher = {Springer Nature}, title = {{Additional file 2 of multi-method genome- and epigenome-wide studies of inflammatory protein levels in healthy older adults}}, doi = {10.6084/m9.figshare.12629697.v1}, year = {2020}, } @misc{9708, abstract = {This research data supports 'Hard antinodal gap revealed by quantum oscillations in the pseudogap regime of underdoped high-Tc superconductors'. A Readme file for plotting each figure is provided.}, author = {Hartstein, Mate and Hsu, Yu-Te and Modic, Kimberly A and Porras, Juan and Loew, Toshinao and Le Tacon, Matthieu and Zuo, Huakun and Wang, Jinhua and Zhu, Zengwei and Chan, Mun and McDonald, Ross and Lonzarich, Gilbert and Keimer, Bernhard and Sebastian, Suchitra and Harrison, Neil}, publisher = {Apollo - University of Cambridge}, title = {{Accompanying dataset for 'Hard antinodal gap revealed by quantum oscillations in the pseudogap regime of underdoped high-Tc superconductors'}}, doi = {10.17863/cam.50169}, year = {2020}, } @misc{9713, abstract = {Additional analyses of the trajectories}, author = {Gupta, Chitrak and Khaniya, Umesh and Chan, Chun Kit and Dehez, Francois and Shekhar, Mrinal and Gunner, M.R. and Sazanov, Leonid A and Chipot, Christophe and Singharoy, Abhishek}, publisher = {American Chemical Society }, title = {{Supporting information}}, doi = {10.1021/jacs.9b13450.s001}, year = {2020}, } @unpublished{9750, abstract = {Tension of the actomyosin cell cortex plays a key role in determining cell-cell contact growth and size. The level of cortical tension outside of the cell-cell contact, when pulling at the contact edge, scales with the total size to which a cell-cell contact can grow1,2. Here we show in zebrafish primary germ layer progenitor cells that this monotonic relationship only applies to a narrow range of cortical tension increase, and that above a critical threshold, contact size inversely scales with cortical tension. This switch from cortical tension increasing to decreasing progenitor cell-cell contact size is caused by cortical tension promoting E-cadherin anchoring to the actomyosin cytoskeleton, thereby increasing clustering and stability of E-cadherin at the contact. Once tension-mediated E-cadherin stabilization at the contact exceeds a critical threshold level, the rate by which the contact expands in response to pulling forces from the cortex sharply drops, leading to smaller contacts at physiologically relevant timescales of contact formation. Thus, the activity of cortical tension in expanding cell-cell contact size is limited by tension stabilizing E-cadherin-actin complexes at the contact.}, author = {Slovakova, Jana and Sikora, Mateusz K and Caballero Mancebo, Silvia and Krens, Gabriel and Kaufmann, Walter and Huljev, Karla and Heisenberg, Carl-Philipp J}, booktitle = {bioRxiv}, pages = {41}, publisher = {Cold Spring Harbor Laboratory}, title = {{Tension-dependent stabilization of E-cadherin limits cell-cell contact expansion}}, doi = {10.1101/2020.11.20.391284}, year = {2020}, } @misc{9776, author = {Grah, Rok and Friedlander, Tamar}, publisher = {Public Library of Science}, title = {{Supporting information}}, doi = {10.1371/journal.pcbi.1007642.s001}, year = {2020}, } @misc{9777, author = {Grah, Rok and Friedlander, Tamar}, publisher = {Public Library of Science}, title = {{Maximizing crosstalk}}, doi = {10.1371/journal.pcbi.1007642.s002}, year = {2020}, } @misc{9779, author = {Grah, Rok and Friedlander, Tamar}, publisher = {Public Library of Science}, title = {{Distribution of crosstalk values}}, doi = {10.1371/journal.pcbi.1007642.s003}, year = {2020}, } @misc{9780, abstract = {PADREV : 4,4'-dimethoxy[1,1'-biphenyl]-2,2',5,5'-tetrol Space Group: C 2 (5), Cell: a 24.488(16)Å b 5.981(4)Å c 3.911(3)Å, α 90° β 91.47(3)° γ 90°}, author = {Schlemmer, Werner and Nothdurft, Philipp and Petzold, Alina and Riess, Gisbert and Frühwirt, Philipp and Schmallegger, Max and Gescheidt-Demner, Georg and Fischer, Roland and Freunberger, Stefan Alexander and Kern, Wolfgang and Spirk, Stefan}, publisher = {CCDC}, title = {{CCDC 1991959: Experimental Crystal Structure Determination}}, doi = {10.5517/ccdc.csd.cc24vsrk}, year = {2020}, } @article{9781, abstract = {We consider the Pekar functional on a ball in ℝ3. We prove uniqueness of minimizers, and a quadratic lower bound in terms of the distance to the minimizer. The latter follows from nondegeneracy of the Hessian at the minimum.}, author = {Feliciangeli, Dario and Seiringer, Robert}, issn = {1095-7154}, journal = {SIAM Journal on Mathematical Analysis}, keywords = {Applied Mathematics, Computational Mathematics, Analysis}, number = {1}, pages = {605--622}, publisher = {Society for Industrial & Applied Mathematics }, title = {{Uniqueness and nondegeneracy of minimizers of the Pekar functional on a ball}}, doi = {10.1137/19m126284x}, volume = {52}, year = {2020}, } @misc{9798, abstract = {Fitness interactions between mutations can influence a population’s evolution in many different ways. While epistatic effects are difficult to measure precisely, important information is captured by the mean and variance of log fitnesses for individuals carrying different numbers of mutations. We derive predictions for these quantities from a class of simple fitness landscapes, based on models of optimizing selection on quantitative traits. We also explore extensions to the models, including modular pleiotropy, variable effect sizes, mutational bias and maladaptation of the wild type. We illustrate our approach by reanalysing a large dataset of mutant effects in a yeast snoRNA. Though characterized by some large epistatic effects, these data give a good overall fit to the non-epistatic null model, suggesting that epistasis might have limited influence on the evolutionary dynamics in this system. We also show how the amount of epistasis depends on both the underlying fitness landscape and the distribution of mutations, and so is expected to vary in consistent ways between new mutations, standing variation and fixed mutations.}, author = {Fraisse, Christelle and Welch, John J.}, publisher = {Royal Society of London}, title = {{Simulation code for Fig S2 from the distribution of epistasis on simple fitness landscapes}}, doi = {10.6084/m9.figshare.7957472.v1}, year = {2020}, } @misc{9799, abstract = {Fitness interactions between mutations can influence a population’s evolution in many different ways. While epistatic effects are difficult to measure precisely, important information is captured by the mean and variance of log fitnesses for individuals carrying different numbers of mutations. We derive predictions for these quantities from a class of simple fitness landscapes, based on models of optimizing selection on quantitative traits. We also explore extensions to the models, including modular pleiotropy, variable effect sizes, mutational bias and maladaptation of the wild type. We illustrate our approach by reanalysing a large dataset of mutant effects in a yeast snoRNA. Though characterized by some large epistatic effects, these data give a good overall fit to the non-epistatic null model, suggesting that epistasis might have limited influence on the evolutionary dynamics in this system. We also show how the amount of epistasis depends on both the underlying fitness landscape and the distribution of mutations, and so is expected to vary in consistent ways between new mutations, standing variation and fixed mutations.}, author = {Fraisse, Christelle and Welch, John J.}, publisher = {Royal Society of London}, title = {{Simulation code for Fig S1 from the distribution of epistasis on simple fitness landscapes}}, doi = {10.6084/m9.figshare.7957469.v1}, year = {2020}, } @misc{9814, abstract = {Data and mathematica notebooks for plotting figures from Language learning with communication between learners}, author = {Ibsen-Jensen, Rasmus and Tkadlec, Josef and Chatterjee, Krishnendu and Nowak, Martin}, publisher = {Royal Society}, title = {{Data and mathematica notebooks for plotting figures from language learning with communication between learners from language acquisition with communication between learners}}, doi = {10.6084/m9.figshare.5973013.v1}, year = {2020}, } @misc{9878, author = {Gupta, Chitrak and Khaniya, Umesh and Chan, Chun Kit and Dehez, Francois and Shekhar, Mrinal and Gunner, M.R. and Sazanov, Leonid A and Chipot, Christophe and Singharoy, Abhishek}, publisher = {American Chemical Society}, title = {{Movies}}, doi = {10.1021/jacs.9b13450.s002}, year = {2020}, } @misc{9885, abstract = {Data obtained from the fine-grained simulations used in Figures 2-5, data obtained from the coarse-grained numerical calculations used in Figure 6, and a sample script for the fine-grained simulation as a Jupyter notebook (ZIP)}, author = {Ucar, Mehmet C and Lipowsky, Reinhard}, publisher = {American Chemical Society }, title = {{MURL_Dataz}}, doi = {10.1021/acs.nanolett.9b04445.s002}, year = {2020}, } @article{27, abstract = {The cerebral cortex is composed of a large variety of distinct cell-types including projection neurons, interneurons and glial cells which emerge from distinct neural stem cell (NSC) lineages. The vast majority of cortical projection neurons and certain classes of glial cells are generated by radial glial progenitor cells (RGPs) in a highly orchestrated manner. Recent studies employing single cell analysis and clonal lineage tracing suggest that NSC and RGP lineage progression are regulated in a profound deterministic manner. In this review we focus on recent advances based mainly on correlative phenotypic data emerging from functional genetic studies in mice. We establish hypotheses to test in future research and outline a conceptual framework how epigenetic cues modulate the generation of cell-type diversity during cortical development. This article is protected by copyright. All rights reserved.}, author = {Amberg, Nicole and Laukoter, Susanne and Hippenmeyer, Simon}, journal = {Journal of Neurochemistry}, number = {1}, pages = {12--26}, publisher = {Wiley}, title = {{Epigenetic cues modulating the generation of cell type diversity in the cerebral cortex}}, doi = {10.1111/jnc.14601}, volume = {149}, year = {2019}, } @article{301, abstract = {A representation formula for solutions of stochastic partial differential equations with Dirichlet boundary conditions is proved. The scope of our setting is wide enough to cover the general situation when the backward characteristics that appear in the usual formulation are not even defined in the Itô sense.}, author = {Gerencser, Mate and Gyöngy, István}, journal = {Stochastic Processes and their Applications}, number = {3}, pages = {995--1012}, publisher = {Elsevier}, title = {{A Feynman–Kac formula for stochastic Dirichlet problems}}, doi = {10.1016/j.spa.2018.04.003}, volume = {129}, year = {2019}, } @article{319, abstract = {We study spaces of modelled distributions with singular behaviour near the boundary of a domain that, in the context of the theory of regularity structures, allow one to give robust solution theories for singular stochastic PDEs with boundary conditions. The calculus of modelled distributions established in Hairer (Invent Math 198(2):269–504, 2014. https://doi.org/10.1007/s00222-014-0505-4) is extended to this setting. We formulate and solve fixed point problems in these spaces with a class of kernels that is sufficiently large to cover in particular the Dirichlet and Neumann heat kernels. These results are then used to provide solution theories for the KPZ equation with Dirichlet and Neumann boundary conditions and for the 2D generalised parabolic Anderson model with Dirichlet boundary conditions. In the case of the KPZ equation with Neumann boundary conditions, we show that, depending on the class of mollifiers one considers, a “boundary renormalisation” takes place. In other words, there are situations in which a certain boundary condition is applied to an approximation to the KPZ equation, but the limiting process is the Hopf–Cole solution to the KPZ equation with a different boundary condition.}, author = {Gerencser, Mate and Hairer, Martin}, issn = {14322064}, journal = {Probability Theory and Related Fields}, number = {3-4}, pages = {697–758}, publisher = {Springer}, title = {{Singular SPDEs in domains with boundaries}}, doi = {10.1007/s00440-018-0841-1}, volume = {173}, year = {2019}, } @article{10874, abstract = {In this article we prove an analogue of a theorem of Lachaud, Ritzenthaler, and Zykin, which allows us to connect invariants of binary octics to Siegel modular forms of genus 3. We use this connection to show that certain modular functions, when restricted to the hyperelliptic locus, assume values whose denominators are products of powers of primes of bad reduction for the associated hyperelliptic curves. We illustrate our theorem with explicit computations. This work is motivated by the study of the values of these modular functions at CM points of the Siegel upper half-space, which, if their denominators are known, can be used to effectively compute models of (hyperelliptic, in our case) curves with CM.}, author = {Ionica, Sorina and Kılıçer, Pınar and Lauter, Kristin and Lorenzo García, Elisa and Manzateanu, Maria-Adelina and Massierer, Maike and Vincent, Christelle}, issn = {2363-9555}, journal = {Research in Number Theory}, keywords = {Algebra and Number Theory}, publisher = {Springer Nature}, title = {{Modular invariants for genus 3 hyperelliptic curves}}, doi = {10.1007/s40993-018-0146-6}, volume = {5}, year = {2019}, }