bluuebunny/crossref_metadata_2025_split huggingface dataset:
De novo transcriptomic characterization of Betta splendens for identifying sex-biased genes potentially involved in aggressive behavior modulation and EST-SSR maker development
Authors: Yang Wei , Wang Yaorong , Zhu Chunhua , Li Guangli , Huang Hai , Chen Huapu 
Published: June 2018

AbstractBetta splendens is not only a commercially important labyrinth fish but also a nice research model for understanding the biological underpinnings of aggressive behavior. However, the shortage of basic genetic resource severely inhibits investigations on the molecular mechanism in sexual dimorphism of aggressive behavior typicality, which are essential for further behavior-related studies. There is a lack of knowledge regarding the functional genes involved in aggression expression. The scarce marker resource also impedes research progress of population genetics and genomics. In order to enrich genetic data and sequence resources, transcriptomic analysis was conducted for mature B. splendens using a multiple-tissues mixing strategy. A total of 105,505,486 clean reads were obtained and by de novo assembly, 69,836 unigenes were generated. Of which, 35,751 unigenes were annotated in at least one of queried databases. The differential expression analysis resulted in 17,683 transcripts differentially expressed between males and females. Plentiful sex-biased genes involved in aggression exhibition were identified via a screening from Gene Ontology terms and Kyoto Encyclopedia of Genes and Genomes pathways, such as htr, drd, gabr, cyp11a1, cyp17a1, hsd17b3, dax1, sf-1, hsd17b7, gsdf1 and fem1c. These putative genes would make good starting points for profound mechanical exploration on aggressive behavioral regulation. Moreover, 12,751 simple sequence repeats were detected from 9,617 unigenes for marker development. Nineteen of the 100 randomly selected primer pairs were demonstrated to be polymorphic. The large amount of transcript sequences will considerably increase available genomic information for gene mining and function analysis, and contribute valuable microsatellite marker resources to in-depth studies on molecular genetics and genomics in the future.
Alien Species of Fish in the Littoral of Volga and Kama Reservoirs (Results of Complex Expeditions of IBIW RAS in 2005-2017)
Authors: Karabanov D.P. , Pavlov D.D. , Bazarov M.I. , Borovikova E.A. , Gerasimov Yu.V. , Kodukhova Yu.V. , Smirnov A.K. , Stolbunov I.A. 
Published: June 2018

abstractThe paper provides information on alien species of fish caught in the coastal waters of the Volga and Kama river reservoirs. The material was collected during complex ship expeditions of the IBIW RAS in 2005-2017. We have identified habitats and estimated the relative abundance of mass alien species of the Volga-Kama region.
Probing Protein Allostery as a Residue-specific Concept via Residue Perturbation Maps
Authors: Hayatshahi Hamed S , Ahuactzin Emilio , Tao Peng , Wang Shouyi , Liu Jin 
Published: June 2018

AbstractAllosteric regulation is a well-established phenomenon classically defined as conformational or dynamical change of a small number of allosteric residues of the protein upon allosteric effector binding at a distance. Here, we developed a novel approach to delineate allosteric effects in proteins. In this approach, we applied robust machine learning methods, including Deep Neural Network and Random Forest, on extensive molecular dynamics (MD) simulations to distinguish otherwise similar allosteric states of proteins. Using PDZ3 domain of PDS-95 as a model protein, we demonstrated that the allosteric effects could be represented as residue-specific properties through two-dimensional property-residue maps, which we refer as “residue perturbation maps”. These maps were constructed through two machine learning methods and could accurately describe how different properties of various residues are affected upon allosteric perturbation on protein. Based on the “residue perturbation maps”, we propose allostery as a residue-specific concept, suggesting all residues could be considered as allosteric residues because each residue “senses” the allosteric events through perturbation of its one or multiple attributes in a quantitatively unique way. The “residue perturbation maps” could be used to fingerprint a protein based on the unique patterns of residue perturbations upon binding events, providing a novel way to systematically describe the protein allosteric effects of each residue upon perturbation.Author SummaryAllostery is protein regulation at distance. A perturbation at one site of the protein could distantly affect another site. The residues involved in these sites are considered as allosteric residues. The allostery concept has been widely used to understand protein mechanisms and to design allosteric drugs. It is long believed only a small number of residues are allosteric residues. Here, we argue that all residues in a protein are allosteric residues. Upon the perturbation of the allosteric events, the different properties of each residue are affected at the distinct extend. We used hybrid models including molecular dynamics simulations and machine learning components to reveal that not only many properties of residues are affected upon ligand binding, but also each residue is affected through perturbation of its various properties, which makes the residue distinguishable from other residues. According to our findings in a model protein, we defined a “residue perturbation map” as a two-dimensional map that fingerprint a protein based on the extent of perturbation in different properties of all its residues in a quantitative fashion. This “residue perturbation map” provides a novel way to systematically describe the protein allosteric effects of each residue upon perturbation.
Genomic analysis of fast expanding bacteria reveals new molecular adaptive mechanisms
Authors: Bosshard Lars , Peischl Stephan , Ackermann Martin , Excoffier Laurent 
Published: June 2018

AbstractBacterial populations have been shown to accumulate deleterious mutations during spatial expansions that overall decrease their fitness and ability to grow. However, it is unclear if and how they can respond to selection in face of this mutation load. We examine here if artificial selection can counteract the negative effects of range expansions. We investigated the molecular evolution of 20 lines (SEL) selected for fast expansions and compared them to 20 lines without artificial selection (CONTROL). We find that all 20 SEL lines have been able to increase their expansion speed relative to the ancestral line, unlike CONTROL lines, showing that enough beneficial mutations are produced during spatial expansions to counteract the negative effect of expansion load. Importantly, SEL and CONTROL lines have similar numbers of mutations indicating that they evolved for the same number of generations and that increased fitness is not due to a purging of deleterious mutations. We find that loss of function (LOF) mutations are better at explaining the increased expansion speed of SEL lines than non-synonymous mutations or a combination of the two. Interestingly, most LOF mutations are found in simple sequence repeats located in genes involved in gene regulation and gene expression. We postulate that such potentially reversible mutations could play a major role in the rapid adaptation of bacteria to changing environmental conditions by shutting down expensive genes and adjusting gene expression.Author SummaryWe investigated if strong artificial selection for fast expansion can counteract the negative effects of range expansion which had been shown to lead to an accumulation of deleterious mutations. This experiments showed that i) an increase in expansion speed could occur if bacteria were selected from the largest protruding sectors, and ii) that artificially selected bacterial lines accumulated about the same number of mutations than simply expanding line suggesting that the observed increased fitness is not due to increased purifying selection where deleterious mutations would have been removed in fast growing lines. We find that loss of function (LOF) mutations are best explaining the observed increased expansion speed in selected lines. These mutations, which are known to play an important role in adaptive processes in bacterial populations, frequently consist in small insertion-deletions in simple sequence repeats, and are thus relatively easily reversible. They could thus act as switches that can reversibly shut down genes. Our results therefore suggest that shutting down expensive genes and adjusting gene expression are important for adaptive processes during range expansion.
Evolutionary epidemiology ofStreptococcus iniae: linking mutation rate dynamics with adaptation to novel immunological landscapes
Authors: Silayeva Oleksandra , Engelstädter Jan , Barnes Andrew C 
Published: June 2018

AbstractPathogens continuously adapt to changing host environments where variation in their virulence and antigenicity is critical to their long-term evolutionary success. The emergence of novel variants is accelerated in microbial mutator strains (mutators) deficient in DNA repair genes, most often from mismatch repair and oxidised-guanine repair systems (MMR and OG respectively). Bacterial MMR/OG mutants are abundant in clinical samples and show increased adaptive potential in experimental infection models, yet the role of mutators in the epidemiology and evolution of infectious disease is not well understood. Here we investigated the role of mutation rate dynamics in the evolution of a broad host range pathogen,Streptococcus iniae, using a set of 80 strains isolated globally over 40 years. We have resolved phylogenetic relationships using non-recombinant core genome variants, measuredin vivomutation rates by fluctuation analysis, identified variation in major MMR/OG genes and their regulatory regions, and phenotyped the major traits determining virulence in streptococci. We found that both mutation rate and MMR/OG genotype are remarkably conserved within phylogenetic clades but significantly differ between major phylogenetic lineages. Further, variation in MMR/OG loci correlates with occurrence of atypical virulence-associated phenotypes, infection in atypical hosts (mammals), and atypical tissue of a vaccinated primary hosts (barramundi bone). These findings suggest that mutators are likely to facilitate adaptations preceding major diversification events, and may promote emergence of variation permitting colonisation of a novel host tissue, novel host taxa (host jumps), and immune-escape in the vaccinated host.
PRL-1 is required for neuroprotection against olfactory CO2 stimulation in Drosophila
Authors: Guo Pengfei , Xu Xiao , Wang Fang , Yuan Xin , Tu Yinqi , Zhang Bei , Zheng Huimei , Yu Danqing , Ge Wanzhong , Gong Zhefeng , Gao Weiqiang , Yang Xiaohang , Xi Yongmei 
Published: June 2018

AbstractThe Mammalian phosphatase of regenerating liver (PRL) family is primarily recognized for its oncogenic properties. Here we found that in Drosophila, loss of prl-1 resulted in CO2-induced brain disorder presented as irreversible wing hold up with enhancement of Ca2+ responses at the neuron synaptic terminals. Overexpression of Prl-1 in the nervous system could rescue the mutant phenotype. We show that Prl-1 is particularly expressed in CO2-responsive neural circuit and the higher brain centers. Ablation of the CO2 olfactory receptor, Gr21a, suppressed the mutant phenotype, suggesting that CO2 acts as a neuropathological substrate in absence of Prl-1. Further studies found that the wing hold up is an obvious consequence upon knockdown of Uex, a magnesium transporter, which directly interacts with Prl-1. Conditional expression of Uex in the nervous system could rescue the phenotype of prl-1 mutants. We demonstrate that Uex acts genetically downstream of Prl-1. Our findings provide important insights into mechanisms of Prl-1 protection against olfactory CO2 stimulation induced brain disorder at the level of detailed neural circuits and functional molecular connections.
Lag Effects in Primate Brain Size Evolution: A Re-Evaluation
Authors: Dunbar R.I.M. 
Published: June 2018

AbstractThe question as to whether there is a lag between brain and body mass evolution was ostensibly solved two decades ago by Deaner & Nunn (1999) who used phylogenetic methods to show that there was no evidence to suggest that changes in brain size lagged behind changes in body size. However, their assumption that body size would always change ahead of brain size is open to question. In addition, many of their datapoints are confounded by grade shift effects. A reanalysis of their data controlling for these confounds shows that there is in fact a strong lag effect, but that the direction of the lag is the reverse of that originally assumed: brain size typically changes first, and does so under selection from changes in group size. The data suggest that it takes about 2.0 million years for body size to converge back onto the conventional allometric relationship with brain size. In the meantime, species that have increased brain size are likely to incur a significant energy cost that must be met from elsewhere. I show that they seem to do so by changing to a more nutrient-rich diet.
HmtVar: a brand-new resource for human mitochondrial variations and pathogenicity data
Authors: Preste R. , Vitale O. , Clima R. , Attimonelli M. 
Published: June 2018

AbstractHuman mitochondrial data are currently of great interest for both clinicians and researchers, due to the involvement of mitochondria in a number of physiological and pathological processes. Thanks to new sequencing technologies and modern databases, the huge amount of information about mitochondrial genome variability can be exploited to gain interesting insights into the relationship between DNA variants, phenotypes and diseases. For this reason, we have developed the new HmtVar resource, a variant-focused database which allows to explore a dataset of over 30000 human mitochondrial variants together with their pathogenicity prediction. Mitochondrial variation data, initially gathered from the HmtDB platform, are further integrated with in-house pathogenicity assessments based on well-established variants pathogenicity evaluation criteria, as well as with a set of additional annotations from third-party resources. This approach led to a comprehensive collection of information of crucial importance for human mitochondrial variation studies and investigation of common and rare diseases in which the mitochondrion is involved to some extent.HmtVar is accessible at https://www.hmtvar.uniba.it and its data can be retrieved using either a web interface through the Query page or a state-of-the-art API for programmatic access.
The exon junction complex undergoes a compositional switch that alters mRNP structure and nonsense-mediated mRNA decay activity
Authors: Mabin Justin W. , Woodward Lauren A. , Patton Robert , Yi Zhongxia , Jia Mengxuan , Wysocki Vicki , Bundschuh Ralf , Singh Guramrit 
Published: June 2018

SUMMARYThe exon junction complex (EJC) deposited upstream of mRNA exon junctions shapes structure, composition and fate of spliced mRNA ribonucleoprotein particles (mRNPs). To achieve this, the EJC core nucleates assembly of a dynamic shell of peripheral proteins that function in diverse post-transcriptional processes. To illuminate consequences of EJC composition change, we purified EJCs from human cells via peripheral proteins RNPS1 and CASC3. We show that EJC originates as an SR-rich mega-dalton sized RNP that contains RNPS1 but lacks CASC3. After mRNP export to the cytoplasm and before translation, the EJC undergoes a remarkable compositional and structural remodeling into an SR-devoid monomeric complex that contains CASC3. Surprisingly, RNPS1 is important for nonsense-mediated mRNA decay (NMD) in general whereas CASC3 is needed for NMD of only select mRNAs. The promotion of switch to CASC3-EJC slows down NMD. Overall, the EJC compositional switch dramatically alters mRNP structure and specifies two distinct phases of EJC-dependent NMD.
MBIR: A Cryo-electron Tomography 3D Reconstruction Method that Effectively Minimizes Missing Wedge Artifacts and Restores Missing Information
Authors: Yan Rui , Venkatakrishnan Singanallur V. , Liu Jun , Bouman Charles A. , Jiang Wen 
Published: June 2018

AbstractCryo-Electron Tomography (cryo-ET) has become an essential technique in revealing cellular and macromolecular assembly structures in their native states. However, due to radiation damage and the limited tilt range, cryo-ET suffers from low contrast and missing wedge artifacts, which limits the tomograms to low resolution and hinders further biological interpretation. In this study, we applied the Model-Based Iterative Reconstruction (MBIR) method to obtain tomographic 3D reconstructions of experimental cryo-ET datasets and demonstrated the advantages of MBIR in contrast improvement, missing wedge artifacts reduction, and missing information restoration compared with other reconstruction approaches. Considering the outstanding reconstruction quality, MBIR has a great potential in the determination of high resolution biological structures with cryo-ET.
Differential gene expression and gene-set enrichment analysis in Caco-2 monolayers during a 30-day timeline with Dexamethasone exposure
Authors: Robinson J.M. , Turkington S. , Abey S.A. , Kenea N. , Henderson W.A. 
Published: June 2018

AbstractThe Caco-2 cell line has served a historically important role as in vitro model for molecular and cellular biology of polarized intestinal epithelia, including for effects of glucocorticoid hormone Dexamethasone. Glucocorticoid hormones modulate the endogenous stress response and are important pharmaceuticals for inflammatory diseases including IBD, yet while they significantly affect immune cells, less is known about their specific effects upon epithelial cells and specific effect on epithelial permeability. Previous research showed that DEX exposure does not immediately produce a quantitative effect, but only after a prolonged treatment >10 days. Culture age itself causes marked effects in these non-renewing cell layers which acts as a confounding variable for observed DEX results. To improve resolution of GC-responsive gene expression in this context, we tested polarized Caco-2 monolayer cultures during at 30-day timecourse, with ~15-days of continuous Dexamethasone exposure. We tested differential gene expression using a 250-plex gene expression panel with the Nanostring nCounter® system, with multiple replicates collected periodically over the timecourse. Gene panel was selectively enriched a-priori for KEGG pathway annotations from tight-junction, actin cytoskeleton regulation, colorectal cancer pathways and others, allowing highly focused, gene-set pathway enrichment analyses. Nanostring nSolver™ data modelling algorithm uses an optimization algorithm and mixture negative binomial model to factor for Time and DEX covariate effects during determination of DE. Analysis identifies strong, culture age-associated “EMT-like” signature with upregulation of actomyosin contraction and integrins, while DEX treatment is associated with a subtler, yet significant counter-signal with suppression of actomyosin genes, and selective DE for different RTKs.
Placental epigenetics for evaluation of fetal congenital heart defects: Ventricular septal defect (VSD)
Authors: Bahado-Singh Ray , Albayrak Samet , Zafra Rita , Baraa Alosh , Veerappa Avinash M , Mahishi Deepthi , Sayed Nazia , Mishra Nitish K , Guda Chittibabu , Ali-Fehmi Rouba , Radhakrishna Uppala 
Published: June 2018

AbstractVentricular Septal Defect (VSD), the most common congenital heart defect, is characterized by a hole in the septum between the right and left ventricles. The pathogenesis of VSD is unknown in most clinical cases. There is a paucity of data relevant to epigenetic changes in VSD. The placenta is a fetal tissue and is a potentially useful surrogate for the evaluation of fetal organ development. To understand epigenetic mechanisms that may play a role in the development of VSD, a genome-wide DNA methylation assay of the placentas of 8 term subjects with isolated VSD and no known or suspected genetic syndromes and 10 normal controls was performed using the Illumina HumanMethylation450 BeadChip assay. The study identified a total of 80 highly accurate potential epigenomic markers in 80 genes for the detection of VSD; area under the receiver operating characteristic curve (AUC ROC) = 1.0 with significant 95% CI (FDR) p-values < 0.05. The biological processes and functions for these differentially methylated genes are known to be associated with heart development or heart disease, including cardiac ventricle development (HEY2, ISL1), heart looping (SRF), cardiac muscle cell differentiation (ACTC1, HEY2), cardiac septum development (ISL1), heart morphogenesis (SRF, HEY2, ISL1, HEYL), Notch signaling pathway (HEY2, HEYL), cardiac chamber development (ISL1), and cardiac muscle tissue development (ACTC1, ISL1). The study also identified eight microRNA genes that have the potential to be biomarkers for the early detection of VSD including miR-191, miR-548F1, miR-148A, miR-423, miR-92B, miR-611, miR-2110, and miR-548H4. To our knowledge this is the first report in which placental analysis has been used for determining the pathogenesis of and predicting CHD.
Remittance and poverty in developing countries
Authors: Masron Tajul Ariffin , Subramaniam Yogeeswari 
Published: June 2018

Purpose
Remittances to developing countries, especially less developed countries, have been growing tremendously as compared to the past few decades. Nevertheless, whether they can be a critical source of poverty alleviation in developing countries is yet to be conclusively studied. Therefore, this study investigates the implications of remittances on poverty in 44 developing countries from 2006 to 2014.

Design/methodology/approach
A dynamic panel estimator is applied to examine remittances – poverty nexus.

Findings
The results provide strong evidence that the level of poverty tends to be lower in countries with a higher flow of remittances. This may be because of the increase in the household incomes of the poor by virtue of the remittance, and/or the money remitted might be channeled to more productive activities, indicating the powerful role of remittances to maintain a sustainable reduction in poverty.

Originality/value
Although there is no direct policy applicable to remittances, several areas might be good to be assisted and improved by the government.