Biology subjects

Venkatesan, A.

Publications and source records attributed to Venkatesan, A..

18 recordsLinked to original sources

bioRxiv2026

Gene regulatory co-expression networks decipher potential lncRNA-miRNA-mRNA interactions modulating transcription regulation in neurodegeneration

Neurodegenerative diseases are complex disorders characterised by progressive neuronal loss and widespread transcriptomic dysregulation; however, the coordinated interactions among coding and non-coding RNAs that contribute to disease progression remain incompletely understood. In this study, RNA-seq datasets from disease-relevant neuronal populations and brain regions representing Alzheimers disease (AD), Parkinsons disease (PD) and amyotrophic lateral sclerosis (ALS) were analysed using an integrative network-based framework. Differential expression analysis coupled with weighted gene co-expression network analysis identified modules significantly correlated with disease and prioritised highly connected hub genes. Integration of these hub genes with curated RNA interaction database enabled the construction of candidate lncRNA-miRNA-mRNA regulatory networks. Functional enrichment analysis revealed Gene Ontology biological processes associated with synaptic signalling, mitochondrial function, RNA metabolism and neuroinflammatory responses across neurodegenerative conditions. The inferred regulatory networks suggested both disease-specific and shared post-transcriptional regulatory modules involving key hub genes and non-coding RNAs. Additionally, putative sequence variants were identified within untranslated regions of selected hub genes, suggesting potential alterations in miRNA-mediated regulations. Therefore, this study provides a systems-level view of transcriptomic dysregulation across major neurodegenerative diseases and identifies candidate regulatory interactions and molecular targets for future functional investigation.

bioinformatics↗

bioRxiv2026

INHIBITION OF LIGAND-DEPENDENT BMP SIGNALING BLUNTS MELANOMA GROWTH

Treatments for advanced melanoma have markedly improved, but a significant proportion of patients still receive little to no survival benefit with standard-of-care therapies due to resistance and relapse1-5. The discovery and development of novel targets and therapies are needed to continue to improve patient outcomes in advanced melanoma. The identification of ligand-dependent BMP signaling that inhibits differentiation and promotes survival of melanoma cells suggests it is a potential therapeutic target that could complement current therapies6. Expression of the BMP ligand GDF6 (a.k.a BMP13) is responsible for this activity, and its expression is correlated with poor outcomes for melanoma patients. Here, we describe a novel monoclonal antibody targeting GDF6 that causes melanoma cell differentiation and death and blunts tumor growth in vivo. Together, these results indicate BMP-directed therapy has significant potential as a novel therapy for patients with advanced melanoma.

Cancer Biology↗

bioRxiv2025

Inducible Calling Cards: Developing Mouse Reagents for Experimentally Controlled Transposon Insertion in vivo.

The piggyBac transposase enables robust forward genetic screens in mice. Further, fusions of piggyBac with specific transcription factors (TFs) enables recovery of recoverable transposons (Calling Cards) for recording location of DNA binding events in vitro and in vivo. Such applications would be enhanced by engineering inducible transposases, such that timing of recording could be precisely controlled in vivo, as has been previously developed in vitro. Here, we tested two approaches for applying inducible Calling Cards (iCC) in the murine brain. We engineered knock-ins of inducible versions of two TFs: Jun, an immediate early gene that serves as a proxy for neural activity, and Sp1, a promiscuous binder of CpG unmethylated regions that indicates active promoters. We fused hyperPiggyBac transposase and a tamoxifen-inducible domain (ERT2) to these TFs and tested the system for efficacy and temporal control of insertions, both in vitro and in vivo. Jun-iCC mice developed normally with no behavioral abnormalities, showed tamoxifen-dependent recording, and captured neural activity during pharmacologically induced seizures. Jun-iCC yields relatively low numbers of insertions, likely due to the transient expression of Jun. In contrast, Sp1-iCC provided substantially higher insertion numbers, but transgenic animals exhibited developmental abnormalities, including reduced viability, anophthalmia, and reduced body weight, suggesting that ERT2 domains may sequester Sp1 and thus significantly impact development. Nonetheless, these inducible Calling Cards mouse lines enable drug-inducible integration of transposon cargo into specific loci in the living mouse. SIGNIFICANCE STATEMENTTransposases, like the more widely used recombinases (Cre, Flp, etc.), enable the integration of a variety of DNA sequences into the genome, but without dependence on LoxP sites. However, few mouse reagents exist for transposases. Cre has been adapted to be drug-inducible, as well as activity-regulated (e.g., FOS-TRAP). Thus, additional applications would become available if transposases could also be drug-controlled and activity-dependent. Further, there may be benefits to targeting integration to specific genomic region types (e.g., promotors). Here, we report results testing mouse lines for two drug-inducible transposase fusions to transcription factors (TF) - the promoter binding SP1, and activity dependent Jun. Both allowed genomic integration, with viability, efficiency, inducibility and targeting varying by TF-fusion.

neuroscience↗

bioRxiv2024

Mitochondrial and Microtubule Defects in Exfoliation Glaucoma

Exfoliation Syndrome (XFS) is an age-related systemic condition characterized by large aggregated fibrillar material deposition in the anterior eye tissues. This aggregate formation and deposition on the aqueous humor outflow pathway are significant risk factors for developing Exfoliation Glaucoma (XFG), a secondary open-angle glaucoma. XFG is a complex, multifactorial late-onset disease that shares common features of neurodegenerative diseases, such as altered cellular processes with increased protein aggregation, impaired protein degradation, and oxidative and cellular stress. XFG patients display decreased mitochondrial membrane potential and mitochondrial DNA deletions. Here, using Tenon Capsule Fibroblasts (TFs) from Normal (No Glaucoma) and XFG patients, we found that XFG TFs have impaired mitochondrial bioenergetics and increased reactive oxygen species (ROS) accumulation. These defects are associated with mitochondrial abnormalities as XFG TFs exhibit smaller mitochondria that contain dysmorphic cristae, with an increase in mitochondrial localization to lysosomes and slowed mitophagy flux. Mitochondrial dysfunction in the XFG TFs was associated with an increase in the dynamics of the microtubule cytoskeleton, decreased acetylated tubulin, and increased HDAC6 activity. Treatment of XFG TFs with a mitophagy inducer, Urolithin A, and a mitochondrial biogenesis inducer, NAD+ precursor, Nicotinamide Ribose, improved mitochondrial bioenergetics and reduced ROS accumulation. Our results demonstrate abnormal mitochondria in XFG TFs and suggest that mitophagy inducers may represent a potential class of therapeutics for reversing mitochondrial dysfunction in XFG patients.

cell biology↗

bioRxiv2024

Discovery of a novel albendazole-ivermectin refractory Trichuris species, T. hominis, in C&ocircte d'Ivoire patients through fecal DNA metabarcoding

Albendazole-ivermectin combination therapy is a promising alternative to benzimidazole monotherapy for Trichuris trichiura control. We used fecal DNA metabarcoding to genetically characterize Trichuris populations in patients from a clinical trial showing lower albendazole-ivermectin efficacy in Cote dIvoire (ERR below 70%) than in Lao PDR and Tanzania (ERR above 98%). ITS-1 and ITS-2 rDNA metabarcoding revealed the entire Cote dIvoire Trichuris population was phylogenetically distinct from T. trichiura in Lao PDR and Tanzania, and more closely related to the porcine parasite Trichuris suis. Complete mitogenomes of eight adult Trichuris from Cote dIvoire confirmed their species-level differentiation. Corresponding Trichuris ITS-1 and ITS-2 sequences in NCBI from individual human patients in Cameroon and Uganda and three captive non-human primates suggest this newly recognized species, T. incognita, is distributed beyond Cote dIvoire and has zoonotic potential. Further work is needed to assess the impact of this Trichuris species on soil transmitted helminth control programs.

genomics↗

bioRxiv2024

Lit-OTAR Framework for Extracting Biological Evidences from Literature

The lit-OTAR framework, developed through a collaboration between Europe PMC and Open Targets, leverages deep learning to revolutionise drug discovery by extracting evidence from scientific literature for drug target identification and validation. This novel framework combines Named Entity Recognition (NER) for identifying gene/protein (target), disease, organism, and chemical/drug within scientific texts, and entity normalisation to map these entities to databases like Ensembl, Experimental Factor Ontology (EFO), and ChEMBL. Continuously operational, it has processed over 39 million abstracts and 4.5 million full-text articles and preprints to date, identifying more than 48.5 million unique associations that significantly help accelerate the drug discovery process and scientific research (> 29.9m distinct target-disease, 11.8m distinct target-drug and 8.3m distinct disease-drug relationships). The results are made accessible through the Open Targets Platform (https://platform.opentargets.org/) as well as Europe PMC website (SciLite web app) and annotations API (https://europepmc.org/annotationsapi).

bioinformatics↗

bioRxiv2023

Lysosomal Degradation Pathways Target Mutant Calreticulin and the Thrombopoietin Receptor in Myeloproliferative Neoplasms

Somatic mutants of calreticulin (CRT) drive myeloproliferative neoplasms (MPNs) via binding to the thrombopoietin receptor (MPL) and aberrant activation of the JAK/STAT pathway. Compared with healthy donors, platelets from MPN patients with CRT mutations display low cell surface MPL. Co-expression of MPL with an MPN-linked CRT mutant (CRTDel52) reduces cell surface MPL expression, indicating the involvement of induced protein degradation, a better understanding of which could lead to new therapies. We show that lysosomal degradation is relevant to the turnover of both CRTDel52 and MPL. Drug-mediated activation of lysosomal degradation reduces CRTDel52 and MPL expression, with parallel inhibition of CRTDel52-induced cell proliferation and stem cell colony formation. Thus, reduced surface MPL, a marker of platelets from MPN patients with CRT mutations, results from mutant CRT-induced lysosomal degradation of MPL. Drug-induced activation of lysosomal degradation compromises the pathogenic effects of CRTDel52, which can be further exploited for therapeutic interventions.

cancer biology↗

bioRxiv2023

Europe PMC Annotated Full-text Corpus for Gene/Proteins, Diseases and Organisms

Named entity recognition (NER) is a widely used text-mining and natural language processing (NLP) sub-task. In recent years, deep learning methods have superseded traditional dictionary, and rule-based NER approaches. A high-quality dataset is essential to take full advantage of the recent deep learning advancements. While several gold standard corpora for biomedical entities in abstracts exist, only a few are based on full-text research articles. The Europe PMC literature database routinely annotates Gene/Proteins, Diseases and Organisms entities; to transition this pipeline from a dictionary-based to a machine learning-based approach, we have developed a human-annotated full-text corpus for these entities comprising 300 full-text open access research articles. Over 72,000 mentions of biomedical concepts have been identified within approximately 114,000 sentences. This article describes the corpus and details how to access and reuse this open community resource.

bioinformatics↗

bioRxiv2022

Molecular evidence of widespread benzimidazole drug resistance in Ancylostoma caninum from domestic dogs throughout the USA and discovery of a novel isotype-1 β-tubulin benzimidazole resistance mutation.

Ancylostoma caninum is an important zoonotic gastrointestinal nematode of dogs worldwide and a close relative of human hookworms. We recently reported that racing greyhounds in the USA are infected with A. caninum that are commonly resistant to multiple anthelmintics. Benzimidazole resistance in A. caninum in greyhounds was associated with a high frequency of the canonical F167Y(TTC>TAC) isotype-1 {beta}-tubulin mutation. In this work, we show that benzimidazole resistance is remarkably widespread in A. caninum from domestic dogs across the USA. First, we identified and showed the functional significance of a novel benzimidazole isotype-1 {beta}-tubulin resistance mutation, Q134H(CAA>CAT). Several benzimidazole resistant A. caninum isolates from greyhounds with a low frequency of the F167Y(TTC>TAC) mutation had a high frequency of a Q134H(CAA>CAT) mutation not previously reported from any eukaryotic pathogen in the field. Structural modeling predicted that the Q134 residue is directly involved in benzimidazole drug binding and that the 134H substitution would significantly reduce binding affinity. Introduction of the Q134H substitution into the C. elegans {beta}-tubulin gene ben-1, by CRISPR-Cas9 editing, conferred similar levels of resistance as a ben-1 null allele. Deep amplicon sequencing on A. caninum eggs from 685 hookworm positive pet dog fecal samples revealed that both mutations were widespread across the USA, often at high frequency, with prevalences of 49.7% (overall frequency 54.0%) and 31.1% (overall frequency 16.4%) for F167Y(TTC>TAC) and Q134H(CAA>CAT), respectively. Canonical codon 198 and 200 benzimidazole resistance mutations were absent. The F167Y(TTC>TAC) mutation had a significantly higher prevalence and frequency in Western USA than in other regions, which we hypothesize is due to differences in refugia. This work has important implications for companion animal parasite control and the potential emergence of drug resistance in human hookworms. Author SummaryAlthough increasingly common in livestock, no reports of widespread anthelmintic resistance are confirmed in any companion animal or human gastrointestinal nematode parasite to date. The canine hookworm is a common intestinal zoonotic parasite of dogs with severe clinical impacts in young dogs, and for which control is dependent on regular anthelmintic use. We recently reported multiple anthelmintic drug resistance in A. caninum isolates from greyhounds derived from multiple locations in the USA likely caused by long standing intensive treatment regimens in kennels. In this study, we investigated benzimidazole resistance in A. caninum in pet dogs across the USA. We also identified and showed the functional significance of a novel benzimidazole isotype-1 {beta}-tubulin resistance mutation in A. caninum from greyhounds that has not been previously reported in the field for any organism. We then determined that this novel mutation, as well as a previously characterized resistance mutation, were present, often at high frequency, in many A. caninum populations across the USA. This study reports the first evidence of widespread drug resistance for any parasitic nematode of companion animals and illustrates the power of molecular approaches to rapidly assess anthelmintic resistance in a region.

genomics↗

bioRxiv2022

Daam1 negatively regulates USP10 activity

The differentiation of fibroblasts into pathological myofibroblasts during wound healing is in part characterized by increased cell surface expression of v-integrins. Our previous studies found that the deubiquitinase (DUB) USP10 removes ubiquitin from v-integrins, leading to cell surface integrin accumulation, subsequent TGF{beta}1 activation, and myofibroblast differentiation. In this study, a yeast-two hybrid screen elucidated a novel binding partner for USP10, the formin, Daam1. The USP10/Daam1 interaction was also supported by proximity ligation assay (PLA) activity. Treatment with TGF{beta}1 significantly increased USP10 and Daam1 protein expression, PLA signal, and co-localization to actin stress fibers. Furthermore, Daam1 siRNA knockdown significantly reduced a) co-precipitation of USP10 and Daam1 on purified actin stress fibers, and b) {beta}1- and {beta}5-integrin ubiquitination resulting in increased v-, {beta}1-, and {beta}5-integrin total protein levels, v integrin recycling to the cell surface, and extracellular fibronectin (FN) organization. Together, our data suggest that Daam1 negatively regulates USP10s DUB activity and subsequently maintains integrin protein homeostasis.

cell biology↗

bioRxiv2021

Multiple drug resistance in hookworms infecting greyhound dogs in the USA

The hookworm Ancylostoma caninum is the most prevalent nematode parasite of dogs. Recently, we confirmed multiple-drug resistance (MDR) in several A. caninum isolates to all anthelmintic drug classes approved for the treatment of hookworms in dogs in the United States (USA). Cases of MDR hookworms appear to be highly overrepresented in greyhounds, suggesting that the MDR worms evolved on racing greyhound farms/kennels. The aims of this study were to evaluate the range of drug-resistant phenotypes and genotypes of the A. caninum infecting greyhounds. Fecal samples from recently retired greyhounds originating from geographically diverse areas of the USA were acquired from two greyhound adoption kennels, one active greyhound racing kennel, and three veterinary practices that work with adoption kennels. Fecal egg counts (FECs) were performed on fecal samples from 219 greyhounds, and despite almost all the dogs having been treated with one or more anthelmintics in the previous two to four weeks, the mean FEC was 822.4 eggs per gram (EPG). Resistance to benzimidazoles and macrocyclic lactones were measured using the egg hatch assay (EHA) and the larval development assay (LDA) respectively. We performed 23 EHA and 22 LDA on either individual or pooled feces, representing 81 animals. Mean and median IC50 and IC95 values for the EHA were 5.3 uM, 3.6 uM, and 24.5 uM, 23.4 uM respectively. For the LDA, mean and median IC50 values were 749.8 nM, >1000 nM respectively. These values range from 62 to 68 times higher than those we measured in our susceptible laboratory isolates. Pre-treatment fecal samples could not be obtained, however, post-treatment samples representing 219 greyhounds were collected. For samples collected <10 days post-treatment with albendazole, moxidectin, or a combination of febantel-pyrantel-moxidectin, the mean FEC were 349, 333, and 835 EPG, respectively. Samples collected 10-21 days post-treatment with albendazole, moxidectin, or pyrantel, yielded mean FEC of 1874, 335, and 600 EPG, respectively. Samples collected >21 days post-treatment with albendazole or moxidectin yielded mean FEC of 1819 and 1117 EPG, respectively. We obtained DNA from hookworm eggs isolated from 70 fecal samples, comprised of 60 individual dogs and 10 pools from multiple dogs. Deep sequencing of the isotype 1 {beta}-tubulin gene revealed the presence of the F167Y (TTC>TAC) resistance polymorphism in 99% of these samples, with 69% having [≥]75% resistant allele frequency. No resistance-associated polymorphisms were seen at any of the other {beta}-tubulin codons previously reported as associated with benzimidazole resistance in Strongylid nematodes. These clinical, in vitro, and genetic data provide strong evidence that racing and recently retired greyhound dogs in the USA are infected with MDR A. caninum at very high levels in terms of both prevalence and infection intensity.

molecular biology↗

bioRxiv2020

Mpl is activated by dimers of MPN-linked calreticulin mutants stabilized by disulfide bonds and ionic interactions

Myeloproliferative neoplasms (MPNs) are frequently driven by insertions and deletions within the gene encoding calreticulin (CRT). CRTDel52 and CRTIns5 are recurrent mutations. Although oncogenic transformation requires both mutated CRT and the myeloproliferative leukemia protein (Mpl), the molecular mechanism of CRT-mediated constitutive activation of Mpl is unknown. Our studies reveal that the novel C-domain of CRTDel52 encodes specificity both for Mpl binding and for disulfide-mediated CRT dimerization. Disulfide-stabilized CRTDel52 dimers and multimers are observed in MPN patient-derived platelet lysates and in transfected mammalian cells. Cysteine mutations within both the novel C-domain (C400A and C404A) and the conserved N-domain (C163A) of CRTDel52 are required to reduce disulfide-mediated dimers and multimers of CRTDel52. Based on these data and published structures of crystalized CRT oligomers, we tested the relevance of ionic interactions between charged residues proximal to C163 at the N-domain dimerization interface. Charge alteration at these residues affected dimerization and multimerization of both wild type and CRTDel52. Elimination of intermolecular disulfides and disruption of ionic interactions at both proposed dimerization interfaces was required to abrogate the ability of CRTDel52 to induce cytokine-independent cell proliferation via Mpl. Based on these findings, we propose a structural model of the Mpl-activating CRTDel52 unit as a covalently-linked dimer that is stabilized by disulfides and ionic interactions at both the C-domain and N-domain. MPNs exploit a natural dimerization interface of CRT combined with C-domain gain-of-functions to achieve cell transformation.

cancer biology↗

bioRxiv2020

Expression of varicella-zoster virus VLT-ORF63 fusion transcript induces broad viral gene expression during reactivation from neuronal latency

Varicella-zoster virus (VZV) establishes lifelong neuronal latency in most humans world-wide, reactivating in one-third to cause herpes zoster and occasionally chronic pain. How VZV establishes, maintains and reactivates from latency is largely unknown. Latent VZV gene expression is restricted to VZV latency-associated transcript (VLT) and open reading frame 63 (ORF63) in naturally VZV-infected human trigeminal ganglia (TG). Notably, these transcript levels positively correlated suggesting co-regulated transcription during latency. Here, we used direct RNA-sequencing to identify fusion transcripts that combine VLT and ORF63 loci (VLT-ORF63) and are expressed during both lytic and latent VZV infections. Furthermore, real-time PCR, RNA in situ hybridization and 5 rapid amplification of cDNA ends (RACE) all confirmed VLT-ORF63, but not canonical ORF63, expression in human TG. During lytic infection, one of the two major VLT-ORF63 isoforms encodes a novel fusion protein combining VLT and ORF63 proteins (pVLT-ORF63). In vitro, VLT is transcribed in latently VZV-infected human sensory neurons, whereas VLT-ORF63 expression is induced by reactivation stimuli. Moreover, the pVLT-ORF63-encoding VLT-ORF63 isoform induced transcription of lytic VZV genes. Collectively, our findings show that VZV expresses a unique set of VLT-ORF63 transcripts, potentially involved in the transition from latency to lytic VZV infection.

microbiology↗

bioRxiv2020

Human stem cell derived sensory neurons are positioned to support varicella zoster virus latency

The neuropathogenesis of varicella-zoster virus (VZV) has been challenging to study due to the strict human tropism of the virus and the resultant difficulties in establishing tractable experimental models. In vivo, sensory neurons of the dorsal root ganglia and trigeminal ganglia serve as cellular niches that support viral latency, and VZV can subsequently reactivate from these cells to cause disease. Whether sensory neurons possess intrinsic properties that position them to serve as a reservoir of viral latency remains unknown. Here, we utilize a robust human sensory neuron system to investigate lytic infection and viral latency. We find that sensory neurons exhibit resistance to lytic infection by VZV. On the other hand, latent infection in sensory neurons is associated with an episomal-like configuration of viral DNA and expression of the VZV latency-associated transcript (VLT), thus closely mirroring the in vivo state. Moreover, despite the relative restriction in lytic infection, we demonstrate that viral reactivation is possible from latently infected sensory neurons. Taken together, our data suggest that human sensory neurons possess intrinsic properties that serve to facilitate their role as a latent reservoir of VZV. IMPORTANCEVaricella-zoster virus (VZV) has infected over 90% of people worldwide. Following primary infection, the virus can remain dormant in the nervous system and may reactivate later in life, with potentially severe consequences. Here, we develop a model of VZV infection in human sensory neurons in order to determine whether these cells are intrinsically positioned to support latency and reactivation. We find that human sensory neurons are relatively resistant to lytic infection, but can support latency and reactivation. Moreover, during in vitro latency human sensory neurons, but not other neurons, express the newly discovered VZV latency-associated transcript (VLT), thus closely mirroring the in vivo latent state. Taken together, these data indicate that human sensory neurons are uniquely positioned to support latency. We anticipate that this human sensory neuron model will serve to facilitate further understanding of the mechanisms of VZV latency and reactivation.

microbiology↗

bioRxiv2019

The ELIXIR Core Data Resources: fundamental infrastructure for the life sciences

MotivationLife science research in academia, industry, agriculture, and the health sector depends critically on free and open data resources. ELIXIR (www.elixir-europe.org), the European Research Infrastructure for life sciences data, has identified a set of Core Data Resources within Europe that are of most fundamental importance for the long-term preservation of biological data. We explore characteristics of their usage, impact and assured funding horizon to assess their value and importance as an infrastructure, to understand sustainability of the infrastructure, and to demonstrate a model for assessing Core Data Resources worldwide. ResultsThe nineteen resources currently designated ELIXIR Core Data Resources form a data infrastructure in Europe which is a subset of the worldwide open life science data infrastructure. We show that, from 2014 to 2018, data managed by the Core Data Resources more than tripled while staff numbers increased by less than a tenth. Additionally, support for the Core Data Resources is precarious: together they have assured funding for less than a third of current staff after four years. Our findings demonstrate the importance of the ELIXIR Core Data Resources as repositories for research data and knowledge, while also demonstrating the uncertain nature of the funding environment for this infrastructure. ELIXIR is working towards longer-term support for the Core Data Resources and, through the Global Biodata Coalition, aims to ensure support for the worldwide life science data resource infrastructure of which the ELIXIR Core Data Resources are a subset. Contactrachel.drysdale@elixir-europe.org Supplementary informationSupplementary data are available at Bioinformatics online.

bioinformatics↗

bioRxiv2018

3D Structural Connectivity In Healthy Adults: Detecting Structural Connections And Their Underlying Substrates For Olfactory Saccadic Pathway

This confirmatory study aimed to unravel the neural structural connectivity of Olfactory-Saccadic pathways extending between Piriform and Entorhinal Cortices to Frontal Eye Field (FEF), and to correlate its functional importance with possible clinical implications, using Diffusion Imaging fiber Tractography. The confirmatory observational analysis used thirty-two healthy adults, ultra-high b-value, diffusion imaging datasets from an Open access platform in Human Connectome Project (HCP). In all the datasets from both the sexes, fibers were traced and the neural structural connectivity was confirmed. The hemispheric differences between male and female subjects were anaNumber of tracts refers to a bundle of fibres having lysed using independent sample t-test. Thus, the study confirmed the structural existences of Olfactory-saccadic pathways that may be involved in influencing the movements of the neck and eyeball gaze (saccadic eye movement), towards the spatial orientation of olfactory stimulus.

neuroscience↗

bioRxiv2018

OLFACTORY SPATIAL ATTENTION: NEURAL STRUCTURAL CONNECTIVITY REVEALED

Different aspects of spatial neglect, the disability to locate the position of the source of an external stimulus, has been studied frequently especially with regards to lack of response to visual stimuli. A modicum of papers fails to elaborate on that of the auditory field and even less conducted on the extraction of spatial information from olfactory stimuli. In this study we attempted to find a structural connection between the Olfactory Cortex (OC) and Temporoparietal Junction (TPJ), in order to suggest that processed olfactory information is carried from OC to TPJ, where the spatial information of the odor maybe acquired. Positive results were attained in all subjects with a lateralization observed in the right hemisphere.\n\nOne Sentence SummaryExistence and hemispherical dominance.

neuroscience↗

bioRxiv2018

Agronomic Linked Data (AgroLD): a Knowledge-based System to Enable Integrative Biology in Agronomy

Recent advances in high-throughput technologies have resulted in a tremendous increase in the amount of omics data produced in plant science. This increase, in conjunction with the heterogeneity and variability of the data, presents a major challenge to adopt an integrative research approach. We are facing an urgent need to effectively integrate and assimilate complementary datasets to understand the biological system as a whole. The Semantic Web offers technologies for the integration of heterogeneous data and their transformation into explicit knowledge thanks to ontologies. We have developed the Agronomic Linked Data (AgroLD - www.agrold.org), a knowledge-based system relying on Semantic Web technologies and exploiting standard domain ontologies, to integrate data about plant species of high interest for the plant science community e.g., rice, wheat, arabidopsis. We present some integration results of the project, which initially focused on genomics, proteomics and phenomics. AgroLD is now an RDF (Resource Description Format) knowledge base of 100M triples created by annotating and integrating more than 50 datasets coming from 10 data sources -such as Gramene.org and TropGeneDB- with 10 ontologies -such as the Gene Ontology and Plant Trait Ontology. Our evaluation results show users appreciate the multiple query modes which support different use cases. AgroLDs objective is to offer a domain specific knowledge platform to solve complex biological and agronomical questions related to the implication of genes/proteins in, for instances, plant disease resistance or high yield traits. We expect the resolution of these questions to facilitate the formulation of new scientific hypotheses to be validated with a knowledge-oriented approach.

bioinformatics↗