bluuebunny/crossref_metadata_2025_split huggingface dataset:
Anthropogenic marine debris and its dynamics across peri-urban and urban mangroves on Penang Island, Malaysia
Authors: Yin Chee Su , Chai Yee Jean , Carey Danielle , Yusup Yusri , Gallagher John Barry 
Published: September 2019

AbstractMangroves act as sinks to a variety of anthropogenic marine debris (AMD) forms. However, knowledge of their distribution and accumulation dynamics is limited. To address this shortfall, abundance, sorting, and diversity parameters of AMD were evaluated across the canopy of Penang’s urban and peri-urban mangroves. Two urban and two peri-urban mangroves were sampled at different periods over 2 months, with differences constrained by possible changes in their wind fields, and neap-spring tidal development. Debris were counted and classified across transects parallel to the coastline at progressively higher water marks. Plastics made up most of the AMD across all sites. More AMD was retained in the urban sites, consistent with their larger resident population density. Diversity of debris forms were consistent with the type of land use and population livelihood in each area. The greatest differences in abundance, diversity, and evenness were recorded between the lower tidal zones and the remaining inner transects consistent with sorting towards the coastal edge in favour of plastic items. Overall, differences across transects and sites suggested: 1) the canopy and root structure within the main body of the mangrove efficiently retained debris with little sorting; and 2) debris deposited closer to the edge is increasingly sorted and lost to the water body in favour of smaller plastic items, for a constant wind field and irrespective of neap-spring phases. The findings show that mangrove areas are vulnerable to a constant build of potentially harmful debris with selective leakage and sorting of materials back to the water body closer to their coastal edges. For Penang Island, the study highlights the areas in need of attention and prioritization, lists the types of debris needing proper management, and will aid in the future monitoring, mitigation and/or rehabilitation of these sensitive ecosystems.
GPU Accelerated Adaptive Banded Event Alignment for Rapid Comparative Nanopore Signal Analysis
Authors: Gamaarachchi Hasindu , Lam Chun Wai , Jayatilaka Gihan , Samarakoon Hiruna , Simpson Jared T. , Smith Martin A. , Parameswaran Sri 
Published: September 2019

AbstractNanopore sequencing has the potential to revolutionise genomics by realising portable, real-time sequencing applications, including point-of-care diagnostics and in-the-field genotyping. Achieving these applications requires efficient bioinformatic algorithms for the analysis of raw nanopore signal data. For instance, comparing raw nanopore signals to a biological reference sequence is a computationally complex task despite leveraging a dynamic programming algorithm for Adaptive Banded Event Alignment (ABEA)—a commonly used approach to polish sequencing data and identify non-standard nucleotides, such as measuring DNA methylation. Here, we parallelise and optimise an implementation of the ABEA algorithm (termed f5c) to efficiently run on heterogeneous CPU-GPU architectures. By optimising memory, compute and load balancing between CPU and GPU, we demonstrate how f5c can perform ~3-5× faster than the original implementation of ABEA in the Nanopolish software package. We also show that f5c enables DNA methylation detection on-the-fly using an embedded System on Chip (SoC) equipped with GPUs. Our work not only demonstrates that complex genomics analyses can be performed on lightweight computing systems, but also benefits High-Performance Computing (HPC). The associated source code for f5c along with GPU optimised ABEA is available at https://github.com/hasindu2008/f5c.
HY5 is not integral to light mediated stomatal development in Arabidopsis
Authors: Zoulias Nicholas , Brown Jordan , Rowe James , Casson Stuart A. 
Published: September 2019

AbstractLight is a crucial signal that regulates many aspects of plant physiology and growth including the development of stomata, the pores in the epidermal surface of the leaf. Light signals positively regulate stomatal development leading to changes in stomatal density and stomatal index (SI; the proportion of cells in the epidermis that are stomata). Both phytochrome and cryptochrome photoreceptors are required to regulate stomatal development in response to light. The transcription factor ELONGATED HYPOCOTYL 5 (HY5) is a key regulator of light signalling, acting downstream of photoreceptors. We hypothesised that HY5 could regulate stomatal development in response to light signals due to the putative presence of HY5 binding sites in the promoter of the STOMAGEN (STOM) gene, which encodes a peptide regulator of stomatal development. Our analysis shows that HY5 does have the potential to regulate the STOM promoter in vitro and that HY5 is expressed in both the epidermis and mesophyll. However, analysis of hy5 and hy5 hyh double mutants (HYH; HY5-HOMOLOG), found that they had normal stomatal development under different light conditions and the expression of stomatal developmental genes was not perturbed following light shift experiments. Analysis of stable lines overexpressing HY5 also showed no change in stomatal development or the expression of stomatal developmental genes. We therefore conclude that whilst HY5 has the potential to regulate the expression of STOM, it does not have a major role in regulating stomatal development in response to light signals.
Compilation of 29-yearpostmortemexaminations identifies major shifts in equine parasite prevalence from 2000 onwards
Authors: Sallé G. , Guillot J. , Tapprest J. , Foucher N. , Sevin C. , Laugier C. 
Published: September 2019

AbstractHorses are infected by a wide range of parasite species that form complex communities. Parasite control imposes significant constraints on parasite communities whose monitoring remains however difficult to track through time.Postmortemexamination is a reliable method to quantify parasite communities. Here, we compiled 1,673 necropsy reports accumulated over 29 years, in the reference necropsy centre from Normandy (France). The burden of non-strongylid species was quantified and the presence of strongylid species was noted. Details of horse deworming history and the cause of death were registered. Building on these data, we investigated the temporal trend in non-strongylids epidemiology and we determined the contribution of parasites to the death of horses throughout the study period. Data analyses revealed the seasonal variations of non-strongylid parasite abundance and reduced worm burden in race horses. Beyond these observations, we found a shift in the species responsible for fatal parasitic infection from the year 2000 onward, whereby fatal cyathostominosis andParascarisspp. infection have replaced death cases caused byS. vulgarisand tapeworms. Concomitant break in the temporal trend of parasite species prevalence was also found within a 10-year window (1998-2007) that has seen the rise ofParascarisspp. and the decline of bothGasterophilusspp. and tapeworms. A few cases of parasite persistence following deworming were identified that all occurred after 2000. Altogether, these findings provide insights into major shifts in non-strongylid parasite prevalence and abundance over the last 29 years. They also underscore the critical importance ofParascarisspp. in young equids.
ArdC protein overpasses the recipient hsdRMS restriction system broadening conjugation host range
Authors: González-Montes Lorena , del Campo Irene , de la Cruz Fernando , Moncalian Gabriel 
Published: September 2019

AbstractPlasmids, when transferred by conjugation, must overpass restriction-modification systems of the recipient cell. We demonstrate that protein ArdC, encoded by broad host range plasmid R388, was required for conjugation from Escherichia coli to Pseudomonas putida, but not from E. coli to E. coli. Surprisingly, expression of ardC was required in the recipient cells, but not in the donor cells. Besides, ardC was not required for conjugation if the hsdRMS system was deleted in P. putida recipient cells. Thus, ArdC has antirestriction activity against HsdRMS system, and consequently broadens R388 plasmid host range. The crystal structure of ArdC was solved both in the absence and in the presence of Mn2+. ArdC is composed of a non-specific ssDNA binding N-terminal domain and a C-terminal metalloprotease domain, although the metalloprotease activity is not needed for antirestriction function. We also observed by RNA-seq that ArdC-dependent conjugation triggers an SOS response in the P. putida recipient cells. Our findings give new insights, and open new questions, into the antirestriction strategies developed by plasmids to counteract bacterial restriction strategies.
FACT mediates cohesin function on chromatin
Authors: Garcia-Luis Jonay , Lazar-Stefanita Luciana , Gutierrez-Escribano Pilar , Thierry Agnes , García Alicia , González Sara , Sánchez Mar , Jarmuz Adam , Montoya Alex , Dore Marian , Kramer Holger , Karimi Mohammad Mehdi , Antequera Francisco , Koszul Romain , Aragon Luis 
Published: September 2019

AbstractCohesin is a key regulator of genome architecture with roles in sister chromatid cohesion 1,2 and the organisation of higher-order structures during interphase 3 and mitosis 4,5. The recruitment and mobility of cohesin complexes on DNA is restricted by nucleosomes 6-8. Here we show that cohesin role in chromosome organisation requires the histone chaperone FACT. Depletion of FACT in metaphase cells affects cohesin stability on chromatin reducing its accumulation at pericentric regions and binding on chromosome arms. Using Hi-C, we show that cohesin-dependent TAD (Topological Associated Domains)-like structures in G1 and metaphase chromosomes are disrupted in the absence of FACT. Surprisingly, sister chromatid cohesion is intact in FACT-depleted cells, although chromosome segregation failure is observed. Our results uncover a role for FACT in genome organisation by facilitating cohesin-dependent compartmentalization of chromosomes into loop domains.
Temperature response of wheat affects final height and the timing of stem elongation under field conditions
Authors: Kronenberg Lukas , Yates Steven , Boer Martin P. , Kirchgessner Norbert , Walter Achim , Hund Andreas 
Published: September 2019

AbstractIn wheat, temperature affects the timing and intensity of stem elongation (SE). Genetic variation for this process is therefore important for adaptation. This study investigates the genetic response to temperature fluctuations during SE and its relationship to phenology and height. Canopy height of 315 wheat genotypes (GABI wheat panel) was scanned twice weekly in the field phenotyping platform (FIP) of ETH Zurich using a LIDAR. Temperature response was modelled using linear regressions between SE and mean temperature in each measurement interval. This led to a temperature–responsive (slope) and a temperature-irresponsive (intercept) component.The temperature response was highly heritable (H2 = 0.81) and positively related to a later start and end of SE as well as final height. Genome-wide association mapping revealed three temperature-responsive and four temperature-irresponsive quantitative trait loci (QTL). Furthermore, putative candidate genes for temperature-response QTL were frequently related to the flowering pathway in A. thaliana, whereas temperature-irresponsive QTLs corresponded with growth and reduced height genes. In combination with Rht and Ppd alleles, these loci, together with the loci for the timing of SE accounted for 71% of the variability in height.This demonstrates how high-throughput field phenotyping combined with environmental covariates can contribute to a smarter selection of climate-resilient crops.HighlightWe measured ambient temperature response of stem elongation in wheat grown under field conditions. The results indicate that temperature response is highly heritable and linked to the flowering pathway.
Cell-type diversity and regionalized gene expression in the planarian intestine revealed by laser-capture microdissection transcriptome profiling
Authors: Forsthoefel David J. , Cejda Nicholas I. , Khan Umair W. , Newmark Phillip A. 
Published: September 2019

AbstractOrgan regeneration requires precise coordination of new cell differentiation and remodeling of uninjured tissue to faithfully re-establish organ morphology and function. An atlas of gene expression and cell types in the uninjured state is therefore an essential pre-requisite for understanding how damage is repaired. Here, we use laser-capture microdissection (LCM) and RNA-Seq to define the transcriptome of the intestine ofSchmidtea mediterranea,a planarian flatworm with exceptional regenerative capacity. Bioinformatic analysis of 1,844 intestine-enriched transcripts suggests extensive conservation of digestive physiology with other animals, including humans. Comparison of the intestinal transcriptome to purified absorptive intestinal cell (phagocyte) and published single-cell expression profiles confirms the identities of known intestinal cell types, and also identifies hundreds of additional transcripts with previously undetected intestinal enrichment. Furthermore, by assessing the expression patterns of 143 transcriptsin situ, we discover unappreciated mediolateral regionalization of gene expression and cell-type diversity, especially among goblet cells. Demonstrating the utility of the intestinal transcriptome, we identify 22 intestine-enriched transcription factors, and find that several have distinct functional roles in the regeneration and maintenance of goblet cells. Furthermore, depletion of goblet cells inhibits planarian feeding and reduces viability. Altogether, our results show that LCM is a viable approach for assessing tissue-specific gene expression in planarians, and provide a new resource for further investigation of digestive tract regeneration, the physiological roles of intestinal cell types, and axial polarity.
Splotch: Robust estimation of aligned spatial temporal gene expression data
Authors: Äijö Tarmo , Maniatis Silas , Vickovic Sanja , Kang Kristy , Cuevas Miguel , Braine Catherine , Phatnani Hemali , Lundeberg Joakim , Bonneau Richard 
Published: September 2019

AbstractSpatial genomics technologies enable new approaches to study how cells interact and function in intact multicellular environments but present a host of technical and computational challenges. Here we describe Splotch, a novel computational framework for the analysis of spatially resolved transcriptomics data. Splotch aligns transcriptomics data from multiple tissue sections and timepoints to generate improved posterior estimates of gene expression. We demonstrate alignment of a large corpus of single-cell RNA-seq data into an automatically generated spatial-temporal coordinate and study optimal design for spatial transcriptomics experiments.
Genetic perturbations of disease risk genes in mice capture transcriptomic signatures of late-onset Alzheimer’s disease
Authors: Pandey Ravi S. , Graham Leah , Uyar Asli , Preuss Christoph , Howell Gareth R. , Carter Gregory W. 
Published: September 2019

ABSTRACTBackgroundNew genetic and genomic resources have identified multiple genetic risk factors for late-onset Alzheimer’s disease (LOAD) and characterized this common dementia at the molecular level. Experimental studies in model organisms can validate these associations and elucidate the links between specific genetic factors and transcriptomic signatures. Animal models based on LOAD-associated genes can potentially connect common genetic variation with LOAD transcriptomes, thereby providing novel insights into basic biological mechanisms underlying the disease.MethodsWe performed RNA-Seq on whole brain samples from a panel of six-month-old female mice, each carrying one of the following mutations: homozygous deletions of Apoe and Clu; hemizygous deletions of Bin1 and Cd2ap; and a transgenic APOEε4. Similar data from a transgenic APP/PS1 model was included for comparison to early-onset variant effects. Weighted gene co-expression network analysis (WGCNA) was used to identify modules of correlated genes and each module was tested for differential expression by strain. We then compared mouse modules with human postmortem brain modules from the Accelerating Medicine’s Partnership for AD (AMP-AD) to determine the LOAD-related processes affected by each genetic risk factor.ResultsMouse modules were significantly enriched in multiple AD-related processes, including immune response, inflammation, lipid processing, endocytosis, and synaptic cell function. WGCNA modules were significantly associated with Apoe−/−, APOEε4, Clu−/−, and APP/PS1 mouse models. Apoe−/−, GFAP-driven APOEε4, and APP/PS1 driven modules overlapped with AMP-AD inflammation and microglial modules; Clu−/− driven modules overlapped with synaptic modules; and APP/PS1 modules separately overlapped with lipid-processing and metabolism modules.ConclusionsThis study of genetic mouse models provides a basis to dissect the role of AD risk genes in relevant AD pathologies. We determined that different genetic perturbations affect different molecular mechanisms comprising AD, and mapped specific effects to each risk gene. Our approach provides a platform for further exploration into the causes and progression of AD by assessing animal models at different ages and/or with different combinations of LOAD risk variants.
Using Bifurcation Theory for Exploring Pain
Authors: Verma Parul , Kienle Achim , Flockerzi Dietrich , Ramkrishna Doraiswami 
Published: September 2019

AbstractPain is a common sensation which inescapably arises due to injuries, as well as, various diseases and disorders. However, for the same intensity of disturbance arising due to the forgoing causes, the threshold for pain sensation and perception varies among individuals. Here, we present a computational approach using bifurcation theory to understand how the pain sensation threshold varies and how it can be controlled, the threshold being quantified by the electrical activity of a pain-sensing neuron. To this end, we explored the bifurcations arising from a mathematical model representing the dynamics of this neuron. Our findings indicate that the bifurcation points are sensitive to specific model parameters. This demonstrates that the pain sensation threshold can change as shown in experimental studies found in literature. Further investigation using our bifurcation approach coupled with experimental studies can facilitate rigorous understanding of pain response mechanism and provide strategies to control the pain sensation threshold.
Induction of Activity Synchronization among Primed Hippocampal Neurons out of Random Dynamics is Key for Trace Memory Formation and Retrieval
Authors: Zhou Yuxin , Qiu Liyan , Wang Haiying , Chen Xuanmao 
Published: September 2019

AbstractMemory is thought to be encoded by sparsely distributed neuronal ensembles in memory-related regions. However, it is unclear how memory-eligible neurons react incrementally during learning to encode trace fear memory, and how they respond to cues to retrieve the memory. We implemented fiber-optic confocal fluorescence endoscopy to directly visualize calcium dynamics of hippocampal CA1 neurons in freely behaving mice, which were subjected to trace fear conditioning. Here we report that the overall activity levels of CA1 principal neurons showed a right-skewed lognormal-like distribution. A small portion of highly active neurons (termed Primed Neurons) exhibited high sensitivity to sensory stimuli and marked activity plasticity. The Primed Neurons maintained random activity status for at least 5 hours in multiple contexts, including those prior to training and prior to recall. Repetitive training induced Primed Neurons to shift from random activity to a well-tuned synchronization. Importantly, the emergence of activity synchronization coincided with the appearance of mouse freezing behaviors. In recall, a partial synchronization among the same population of Primed Neurons was induced from originally random activity, which also coincided with mouse freezing behaviors. Additionally, training-induced synchronization facilitated robust calcium entry into individual Primed Neurons. In contrast, most CA1 neurons stayed silent and did not respond significantly to tone and foot-shock throughout the training and recall testing cycles. In conclusion, highly active Primed Neurons are preferably recruited to encode trace fear memory, and induction of activity synchronization among Primed Neurons out of random dynamics is critical for trace memory formation and memory retrieval.Significance StatementThe overall activity levels of hippocampal principal CA1 neurons show a right-skewed lognormal-like distribution.A small portion of CA1 neurons (termed Primed Neurons) exhibit high activity and marked activity plasticity during learning and recall.Primed Neurons in the hippocampus are preferably recruited to encode trace fear memory, whereas the majority of CA1 neurons show little activity and little activity change during fear conditioning and recall testing.Induction of activity synchronization among Primed Neurons out of random dynamics is critical for trace memory formation and memory retrieval.Training-induced synchronization drastically increases calcium entry into Primed Neurons, which may promote memory consolidation.
QTL mapping of intestinal neutrophil variation and inflammation between threespine stickleback populations reveals links to neurodegenerative disease
Authors: Beck Emily A. , Currey Mark C. , Small Clayton M. , Cresko William A. 
Published: September 2019

AbstractHost selection is often required to foster beneficial microbial symbionts and suppress deleterious pathogens. In animals, the host immune system is at the center of this relationship. Failed host immune system-microbial interactions can result in a persistent inflammatory response in which the immune system indiscriminately attacks resident microbes, and at times the host cells themselves, leading to diseases such as Ulcerative Colitis, Crohn’s Disease, and Psoriasis. Host genetic variation has been linked to both microbiome diversity and to severity of such inflammatory disease states in humans. However, the microbiome and inflammatory states manifest as quantitative traits, which encompass many genes interacting with one another and the environment. The mechanistic relationships among all of these interacting components are still not clear. Developing natural genetic models of host-microbe interactions is therefore fundamental to understanding the complex genetics of these and other diseases. Threespine stickleback (Gasterosteus aculeatus) fish are a tractable model for attacking this problem because of abundant population-level genetic and phenotypic variation in the gut inflammatory response. Previous work in our laboratory identified genetically divergent stickleback populations exhibiting differences in intestinal neutrophil activity. We took advantage of this diversity to genetically map variation in an emblematic element of gut inflammation – intestinal neutrophil recruitment – using an F2-intercross mapping framework. We identified three regions of the genome associated with increased intestinal inflammation containing several promising candidate genes. Within these regions we found candidates in the Coagulation/Complement System, NFkB and MAPK pathways along with several genes associated with neurodegenerative diseases commonly accompanying intestinal inflammation as a secondary symptom. These findings highlight the utility of using naturally genetically diverse ‘evolutionary mutant models’ such as threespine stickleback to better understand interactions among host genetic diversity and microbiome variation in health and disease states.