bluuebunny/crossref_metadata_2025_split huggingface dataset:
Interspecific variation of olfactory preferences in flies, mice, and humans
Authors: Manoel Diogo , Makhlouf Melanie , Scialdone Antonio , Saraiva Luis R. 
Published: July 2018

AbstractAiming to unravel interspecific differences in olfactory preferences, we performed comparative studies of odor valence in flies, mice, and humans. Our analysis revealed that odor preferences of flies correlate positively with the ones of mice and negatively with the ones of humans, but found no evidence supporting the hypothesis that humans and mice prefer the same odors. We further find that odorants eliciting the highest and lowest preferences are often advertising critical biological sources (e.g., food or oviposition sites), suggesting that evolutionary pressures reflecting the ecological needs of each species shape olfactory preferences.
microRNA-dependent regulation of biomechanical genes establishes tissue stiffness homeostasis
Authors: Moro Albertomaria , Discroll Tristan , Armero William , Boraas Liana C. , Kasper Dionna M. , Baeyens Nicolas , Jouy Charlene , Mallikarjun Venkatesh , Swift Joe , Ahn Sang Joon , Lee Donghoon , Zhang Jing , Gu Mengting , Gerstein Mark , Schwart Martin , Nicoli Stefania 
Published: July 2018

SummaryThe mechanical properties of tissues, which are determined primarily by their extracellular matrix (ECM), are largely stable over time despite continual turnover of ECM constituents1,2. These observations imply active homeostasis, where cells sense and adjust rates of matrix synthesis, assembly and degradation to keep matrix and tissue properties within the optimal range. However, the regulatory pathways that mediate this process are essentially unknown3. Genome-wide analyses of endothelial cells revealed abundant microRNA-mediated regulation of cytoskeletal, adhesive and extracellular matrix (CAM) mRNAs. High-throughput assays showed co-transcriptional regulation of microRNA and CAM genes on stiff substrates, which buffers CAM expression. Disruption of global or individual microRNA-dependent suppression of CAM genes induced hyper-adhesive, hyper-contractile phenotypes in multiple systemsin vitro,and increased tissue stiffness in the zebrafish fin-fold during homeostasis and regenerationin vivo.Thus, a network of microRNAs and CAM mRNAs mediate tissue mechanical homeostasis.
ZetaHunter: a reproducible taxonomic classification tool for tracking the ecology of the Zetaproteobacteria and other poorly-resolved taxa
Authors: McAllister Sean M. , Moore Ryan M. , Chan Clara S 
Published: July 2018

AbstractLike many taxa, the Zetaproteobacteria lack well-defined taxonomic divisions, 32 making it difficult to compare between studies. We designed ZetaHunter to reproducibly 33 assign 16S rRNA gene sequences to previously-described OTUs based on a curated 34 database. While ZetaHunter can use any given database, we include a curated 35 classification of publically-available Zetaproteobacteria.
phylostratr: A framework for phylostratigraphy
Authors: Arendsee Zebulun , Li Jing , Singh Urminder , Seetharam Arun , Dorman Karin , Wurtele Eve Syrkin 
Published: July 2018

AbstractMotivationThe goal of phylostratigraphy is to infer the evolutionary origin of each gene in an organism. Currently, there are no general pipelines for this task. We present an R package, phylostratr, to fill this gap, making high-quality phylostratigraphic analysis accessible to non-specialists.ResultsPhylostratigraphic analysis entails searching for homologs within increasingly broad clades. The highest clade that contains all homologs of a gene is that gene’s phylostratum. We have created a general R-based framework, phylostratr, for estimating the phylostratum of every gene in a species. The program can fully automate an analysis: select species for a balanced representation of each strata, retrieve the sequences from UniProt, build BLAST databases, run BLAST, infer homologs for each gene against each subject species, determine phylostrata, and return summaries and diagnostics. phylostratr allows extensive customization. A user may: modify the automatically-generated clade tree or use their own tree; provide custom sequences in place of those automatically retrieved from UniProt; replace BLAST with an alternative algorithm; or tailor the method and sensitivity of the homology inference classifier. phylostratr also offers proteome quality assessments, false-positive diagnostics, and checks for missing organelle genomes. We show the utility of phylostratr through case studies in Arabidopsis thaliana and Saccharomyces cerevisiae.Availabilityphylostratr source code and vignettes are available on GitHub at https://github.com/arendsee/phylostratrContactevewurtele@gmail.com
Nuclear and mitochondrial genomic resources for the meltwater stonefly,Lednia tumanaRicker, 1952 (Plecoptera: Nemouridae)
Authors: Hotaling Scott , Kelley Joanna L. , Weisrock David W. 
Published: July 2018

AbstractWith more than 3,700 described species, stoneflies (Order Plecoptera) are an important component of global aquatic biodiversity. The meltwater stoneflyLednia tumana(Ricker, 1952; Family Nemouridae) is endemic to alpine streams of Glacier National Park and has been petitioned for listing under the U.S. Endangered Species Act (ESA) due to climate change-induced loss of alpine glaciers and snowfields. Here, we presentde novoassemblies of the nuclear (~520 million base pairs [bp]) and mitochondrial (15,014-bp) genomes forL. tumana. TheL. tumananuclear genome is the most complete stonefly genome reported to date, with ~71% of genes present in complete form and more than 4,600 contigs longer than 10-kilobases (kb). TheL. tumanamitochondrial genome is the second for the family Nemouridae and the first from North America. Together, both genomes represent important foundational resources, setting the stage for future efforts to understand the evolution ofL. tumana, stoneflies, and aquatic insects worldwide.
Temperature-mediated inhibition of a bumble bee parasite by an intestinal symbiont
Authors: Palmer-Young Evan C , Raffel Thomas R , McFrederick Quinn S 
Published: July 2018

ABSTRACTCompetition between organisms is often mediated by environmental factors including temperature. In animal intestines, nonpathogenic symbionts compete physically and chemically against pathogens, with consequences for host infection. We used metabolic theory-based models to characterize differential responses to temperature of a bacterial symbiont and a co-occurring trypanosomatid parasite of bumble bees, which regulate body temperature during flight and incubation. We hypothesized that inhibition of parasites by bacterial symbionts would increase with temperature, due to symbionts having higher optimal growth temperatures than parasites.We found that a temperature increase over the range measured in bumble bee colonies would favor symbionts over parasites. As predicted by our hypothesis, symbionts reduced the optimal growth temperature for parasites, both in direct competition and when parasites were exposed to symbiont spent medium. Inhibitory effects of the symbiont increased with temperature, reflecting accelerated growth and acid production by symbionts. Our results indicate that high temperatures, whether due to host endothermy or environmental factors, can enhance the inhibitory effects of symbionts on parasites. Temperature-modulated manipulation of microbiota could be one explanation for fever- and heat-induced reductions of infection in animals, with consequences for diseases of medical and conservation concern.
Risk of disease spillover from dogs to wild carnivores in Kanha Tiger Reserve, India
Authors: Chaudhary V. , Rajput N. , Shrivastav A. B. , Tonkyn D. W. 
Published: July 2018

AbstractMany mammalian carnivore species have been reduced to small, isolated populations by habitat destruction, fragmentation, poaching, and human conflict. Their limited genetic variability and increased exposure to domestic animals such as dogs place them at risk of further losses from infectious diseases. In India, domestic and feral dogs are associated with villages in and around protected areas, and may serve as reservoirs of pathogens to the carnivores within. India’s Kanha Tiger Reserve (KTR) is home to a number of threatened and endangered mammalian carnivores including tiger (Panthera tigris), leopard (Panthera pardus), wolf (Canis lupus), and dhole (Cuon alpinus). It also has more than 150 villages with associated dog populations. We found that dog populations ranged from 14 to 45/village (3.7 to 23.7/km2), and did not vary with village area, human population size, or distance from the KTR’s core area, though they all increased between summer 2014 and winter 2015, primarily through reproduction. No dog tested positive for rabies but seroprevalence levels to three other generalist viral pathogens were high in summer (N=67) and decreased somewhat by winter (N=168): canine parvovirus (83.6% to 68.4%), canine distemper virus (50.7% to 30.4%) and canine adenovirus (41.8% to 30.9%). The declines in seroprevalence were primarily due to new recruitments by birth and these were not yet exposed to the viruses. Wild carnivores frequently entered the villages, as shown by tracks, scats, kills and other indicators, and the dogs are known to leave the villages so that encounters between dogs and wild carnivores may be common. We conclude that there is a large population of unvaccinated dogs in and around Kanha Tiger Reserve, with high levels of seroprevalence to pathogens with broad host ranges and these dogs which interact with wild carnivores, therefore posing a high risk of disease spillover to the wild carnivores.
Candida albicansgenetic background influences mean and heterogeneity of drug responses and genome stability during evolution to fluconazole
Authors: Gerstein Aleeza C. , Berman Judith 
Published: July 2018

AbstractThe importance of within-species diversity in determining the evolutionary potential of a population to evolve drug resistance or tolerance is not well understood, including in eukaryotic pathogens. To examine the influence of genetic background, we evolved replicates of twenty different clinical isolates ofCandida albicans,a human fungal pathogen, in fluconazole, the commonly used antifungal drug. The isolates hailed from the majorC. albicansclades and had different initial levels of drug resistance and tolerance to the drug. The majority of replicates rapidly increased in fitness in the evolutionary environment, with the degree of improvement inversely correlated with ancestral strain fitness in the drug. Improvement was largely restricted to up to the evolutionary level of drug: only 4% of the evolved replicates increased resistance (MIC) above the evolutionary level of drug. Prevalent changes were altered levels of drug tolerance (slow growth of a subpopulation of cells at drug concentrations above the MIC) and increased diversity of genome size. The prevalence and predominant direction of these changes differed in a strain-specific manner but neither correlated directly with ancestral fitness or improvement in fitness. Rather, low ancestral strain fitness was correlated with high levels of heterogeneity in fitness, tolerance, and genome size among evolved replicates. Thus, ancestral strain background is an important determinant in mean improvement to the evolutionary environment as well as the diversity of evolved phenotypes, and the range of possible responses of a pathogen to an antimicrobial drug cannot be captured by in-depth study of a single strain background.ImportanceAntimicrobial resistance is an evolutionary phenomenon with clinical implications. We tested how replicates from diverse strains ofCandida albicans, a prevalent human fungal pathogen, evolve in the commonly-prescribed antifungal drug fluconazole. Replicates on average increased in fitness in the level of drug they were evolved to, with the least fit ancestral strains improving the most. Very few replicates increased resistance above the drug level they were evolved in. Notably, many replicates increased in genome size and changed in drug tolerance (a drug response where a subpopulation of cells grow slowly in high levels of drug) and variability among replicates in fitness, tolerance and genome size was higher in strains that initially were more sensitive to the drug. Genetic background influenced the average degree of adaptation and the evolved variability of many phenotypes, highlighting that different strains from the same species may respond and adapt very differently during adaptation.
Modelling genotypes in their microenvironment to predict single- and multi-cellular behaviour
Authors: Voukantsis Dimitrios , Kahn Kenneth , Hadley Martin , Wilson Rowan , Buffa Francesca M. 
Published: July 2018

ABSTRACTA cell’s phenotype is the set of observable characteristics resulting from the interaction of the genotype with the surrounding environment, determining cell behaviour. Deciphering genotype-phenotype relationships has been crucial to understand normal and disease biology. Analysis of molecular pathways has provided an invaluable tool to such understanding; however, it does typically not consider the physical microenvironment, which is a key determinant of phenotype.In this study, we present a novel modelling framework that enables to study the link between genotype, signalling networks and cell behaviour in a 3D microenvironment. To achieve this we bring together Agent Based Modelling, a powerful computational modelling technique, and gene networks. This combination allows biological hypotheses to be tested in a controlled stepwise fashion, and it lends itself naturally to model a heterogeneous population of cells acting and evolving in a dynamic microenvironment, which is needed to predict the evolution of complex multi-cellular dynamics. Importantly, this enables modelling co-occurring intrinsic perturbations, such as mutations, and extrinsic perturbations, such as nutrients availability, and their interactions.Using cancer as a model system, we illustrate the how this framework delivers a unique opportunity to identify determinants of single-cell behaviour, while uncovering emerging properties of multi-cellular growth.Availability and ImplementationFreely available on the web athttp://www.microc.org. Research Resource Identification Initiative ID (https://scicrunch.org/): SCR 016672
Shared vulnerability for connectome alterations across psychiatric and neurological brain disorders
Authors: de Lange Siemon C. , Scholtens Lianne H. , van den Berg Leonard H. , Boks Marco P. , Bozzali Marco , Cahn Wiepke , Dannlowski Udo , Durston Sarah , Geuze Elbert , van Haren Neeltje E.M. , Hillegers Manon H.J. , Koch Kathrin , Jurado María Ángeles , Mancini Matteo , Marqués-Iturria Idoia , Meinert Susanne , Ophoff Roel A. , Reess Tim J. , Repple Jonathan , Kahn René S. , van den Heuvel Martijn P. ,   for the Alzheimer’s Disease Neuroimaging Initiative
Published: July 2018

AbstractMacroscale white matter pathways form the infrastructure for large-scale communication in the human brain, a prerequisite for healthy brain function. Conversely, disruptions in the brain’s connectivity architecture are thought to play an important role in a wide range of psychiatric and neurological brain disorders. Here we show that especially connections important for global communication and network integration are involved in a wide range of brain disorders. We report on a meta-analytic connectome study comprising in total 895 patients and 1,016 controls across twelve neurological and psychiatric disorders. We extracted disorder connectome fingerprints for each of these twelve disorders, which were then combined into a cross-disorder disconnectivity involvement map, representing the involvement of each brain pathway across brain disorders. Our findings show connections central to the brain’s infrastructure are disproportionally involved across a wide range of disorders. Connections critical for global network communication and integration display high disturbance across disorders, suggesting a general cross-disorder involvement and importance of these pathways in normal function. Taken together, our cross-disorder study suggests a convergence of disconnectivity across disorders to a partially shared disconnectivity substrate of central connections.
The Mediator CDK8-Cyclin C complex modulates vein patterning inDrosophilaby stimulating Mad-dependent transcription
Authors: Li Xiao , Liu Mengmeng , Ren Xingjie , Loncle Nicolas , Wang Qun , Hemba-Waduge Rajitha-Udakara-Sampath , Boube Muriel , Bourbon Henri-Marc G. , Ni Jian-Quan , Ji Jun-Yuan 
Published: July 2018

AbstractDysregulations of CDK8 and its regulatory partner CycC, two subunits of the conserved Mediator complex, have been linked to diverse human diseases such as cancer, thus it is essential to understand the regulatory network mobilizing the CDK8-CycC complex in both normal development and tumorigenesis. To identify upstream regulators or downstream effectors of CDK8, we performed a dominant modifier genetic screen inDrosophilabased on the defects in vein patterning caused by specific depletion or overexpression of CDK8 or CycC in wing imaginal discs. We identified 26 genomic loci whose haploinsufficiency can modify these CDK8-specific phenotypes. Further analysis of two deficiency lines and mutant alleles led us to identify interactions between CDK8-CycC and the components of the Decapentaplegic (Dpp, theDrosophilahomolog of TGFβ) signaling pathway. We observed that CDK8-CycC positively regulates transcription activated by Mad (Mothers against dpp), the primary transcription factor downstream of the Dpp/TGFβ signaling pathway. CDK8 can directly interact with Madin vitrothrough the linker region between the DNA-binding MH1 (Mad homology 1) domain and the carboxy terminal MH2 transactivation domain. Besides CDK8 and CycC, further analyses of other subunits of the Mediator complex have revealed six additional Mediator subunits that are required for Mad-dependent transcription in the wing discs, including Med12, Med13, Med15, Med23, Med24, and Med31. Furthermore, CDK9 and Yorkie also positively regulate Mad-dependent gene expressionin vivo. These results suggest that the Mediator complex may coordinate with other transcription cofactors in regulating Mad-dependent transcription during the wing vein patterning inDrosophila.SignificanceCDK8 is a conserved subunit of the transcription cofactor Mediator complex that bridges transcription factors with RNA Polymerase II in eukaryotes. Here we explore the role of CDK8 inDrosophilaby performing a dominant modifier genetic screen based on vein patterning defects caused by alteration of CDK8-specific activities. We show that components of the Dpp/TGFβ signaling pathway genetically interact with CDK8; CDK8 positively regulates gene expression activated by Mad, the key transcription factor downstream of Dpp/TGFβ signaling, by directly interacting with the linker region of Mad protein. Given the fundamental roles of Dpp/TGFβ signaling in regulating development and its misregulation in various diseases, understanding how Mad/Smad interacts the Mediator complex may have broad implications in understanding and treating these diseases.
Environmentally-induced epigenetic conversion of a piRNA cluster
Authors: Casier Karine , Delmarre Valérie , Gueguen Nathalie , Hermant Catherine , Viodé Elise , Vaury Chantal , Ronsseray Stéphane , Brasset Emilie , Teysset Laure , Boivin Antoine 
Published: July 2018

ABSTRACTTransposable element (TE) activity is repressed in animal gonads by PIWI-interacting RNAs (piRNAs), a class of small RNAs produced by specific loci made of TEs insertions and fragments. Current models propose that these loci are functionally defined by the maternal inheritance of piRNAs produced during the previous generation, raising the question of their first activation in the absence of piRNAs. Taking advantage of an inactive cluster ofP-element derived transgene insertions, we show here that raising flies at high temperature (29°C) instead of 25°C results in a rare but invasive epigenetic conversion of this locus into an active piRNAs producing one. The newly acquired epigenetic state is stable over many generations even when flies are switch back to 25°C. The silencing capacities, piRNA production and chromatin modifications of the cluster are all identical whether conversion occurred by maternal piRNA inheritance or by high temperature. We also demonstrate that in addition to high temperature, a single homologous transgene inserted elsewhere in the genome is required to activate the locus. We thus have identified a minimal system of three components to create a stable piRNA producing locus: 1) a locus with multiple TE derived sequences; 2) an euchromatic copy of these sequences and 3) elevated temperature. Altogether, these data report the first case of the establishment of an active piRNA cluster by environmental changes. It highlights how such variations of species natural habitat can become heritable and shape their epigenome.SIGNIFICANCE STATEMENTRecently, we have witnessed great progress in our understanding of the silencing of Transposable Elements (TEs) by piRNAs, a class of small RNAs produced by piRNA clusters. At each generation, piRNA clusters are supposed to be activated by homologous piRNAs inherited from the mother raising the question of the making of the first piRNAs. Here, we report the birth of a stable and functional piRNA cluster induced by high temperature without maternal inheritance of homologous piRNAs. We propose a minimal system to create a piRNA cluster: a sufficient number of repeated sequences, a euchromatic copy of these sequences and an increase in the production of antisense RNA.
Computational modeling of social face perception in humans: Leveraging the active appearance model
Authors: Guan Jinyan , Ryali Chaitanya K. , Yu Angela J. 
Published: July 2018

AbstractFace processing plays a central role in human social life. Humans readily infer social traits (e.g. attractiveness and trustworthiness) from a stranger’s face. Previous attempts to characterize the facial (physiognomic) features underlying social processing have lacked either systematicity or interpretability. Here, we utilize a statistical framework to tackle this problem, by learning a vector space to represent faces, and a linear mapping from this face space into human social trait judgments. Specifically, we obtain a face space by training the Active Appearance Model on large datasets of face images. Based on human evaluations of numerous social traits on these images, we then use regression to find linear combinations of facial features (what we call Linear Trait Axis, or LTA) that best predict human social judgments. Our model achieves state-of-the-art performance in overall predictive accuracy – comparable to the best convolutional neural network and better than human prediction of other human ratings. To interpret the LTAs, we regress them against a large repertoire of geometric features. To understand the relationship between the facial features that underlie different social, emotional, and demographic traits, we present a novel “dual space analysis” that characterizes the geometric relationship among LTA vectors. It shows that facial features important for social trait perception are largely distinct from those underlying demographic and emotion perception, contrary to previous suggestions that social trait perception is driven by over-generalization of relatively primitive demographic and emotion perception processes. In addition, we present a novel correlation decomposition analysis that quantifies how correlations in trait judgments (e.g. between attractiveness and babyfacedness) independently arise from (1) shared facial features among traits, and (2) correlation in the distribution of facial features in the human population.