Biology subjects

Harris, N.

Publications and source records attributed to Harris, N..

17 recordsLinked to original sources

bioRxiv2026

A repressive regulatory cascade shapes temporal patterning of activity-regulated gene expression in a defined sensory neuron type

Long-term neuronal plasticity is driven by activity-regulated gene (ARG) expression programs that encode stimulus features in a neuron type-specific manner 1-6. ARG programs are typically characterized by rapid induction of immediate early genes (IEGs) without requiring new protein synthesis, followed by expression of secondary response genes regulated by IEG-encoded transcription factors 2,5,7-14. However, the molecular mechanisms that pattern these programs in specific neuron types in vivo in response to physiological stimuli are not fully described. We previously showed that temperature regulates an ARG program in the C. elegans AFD thermosensory neuron pair to drive behavioral plasticity 3,15,16. By profiling AFD following temperature upshifts of varying duration, here we show that ARGs in this neuron exhibit distinct temporal trajectories. Notably, rapidly induced genes do not include known IEGs but are enriched for molecules implicated in signal transduction and navigation. Both rapid and delayed ARG expression require the CMK-1 CaMKI kinase and CRH-1 CREB transcription factor, with CRH-1 acting at both early and late stages. We further define a temporal regulatory cascade in which CREB-dependent rapid induction of the RCAN-1 calcineurin regulator acts in parallel with the MEF-2 transcription factor to repress premature expression of a delayed ARG. Subsequent downregulation of RCAN-1 likely enables CRH-1-dependent ARG expression at later stages. Our results demonstrate that in addition to classical gene-activating transcriptional cascades, ARG-controlled repressive mechanisms also operate to precisely shape the temporal dynamics of an ARG cascade in a sensory neuron type in vivo, and suggest that distinct cell type-specific regulatory pathways operate to drive ARG expression programs across neuron types.

neuroscience↗

bioRxiv2025

Screening of the Pathogen box reveals novel anti blood-feeding compounds

Soil-transmitted helminth (STH) infections such as Necator americanus infect millions globally, and are a major cause of anemia and developmental stunting in low and middle income countries. Blood-feeding hookworms in particular rely on the digestion of host erythrocytes for nutrition and therefore detoxify heme as a byproduct of their parasitism. This dependency on blood feeding and subsequent detoxification renders this pathway as a vulnerable target for therapeutic intervention, particularly as it is the cause of morbidity in those infected. Here we described the continued development and application of a high-throughput in vitro assay using the so-called rodent hookworm Nippostrongylus brasiliensis, a model that shares key traits with N. americanus including blood feeding and hemozoin-like pigment formation. We optimized a fluorescence-based screening cascade to utilise GelGreen as a cost-effective viability stain and screened 400 compounds from the MMV Pathogen Box. Multiple compounds displayed enhanced activity in the presence of blood, suggesting interference with blood-feeding or blood-feeding-induced development. Five hits were selected for further validation, and as proof-of-principle of this screening cascade, all five were well tolerated in vivo at low doses in a murine model. This study therefore demonstrates this method can be used as a tractable and biologically relevant screening approach to identify compounds active against blood-feeding nematodes. Future work can further develop such compounds into lead drug candidates, and be leveraged for comparative parasitology approaches to identify pan-anthelmintic drugs.

microbiology↗

bioRxiv2025

Experience-dependent reconfiguration of receptors at a sensory compartment regulates neuronal plasticity

Neurons continuously adjust their properties as a function of experience. Precise modulation of neuronal responses is achieved by multiple cellular mechanisms that operate over a range of timescales. Primary sensory neurons rapidly adapt their sensitivities via posttranslational mechanisms including regulated trafficking of sensory molecules1-4 but also alter their transcriptional profiles on longer timescales to adapt to persistent sensory stimuli5-8. How diverse transcriptional and posttranscriptional pathways are coordinated in individual sensory neurons to accurately adjust their functions and drive behavioral plasticity is unclear. Here we show that temperature experience modulates both transcription and trafficking of thermoreceptors on different timescales in the C. elegans AFD thermosensory neurons to regulate response plasticity. Expression of the PY motif-containing adaptor protein (PYT-1) as well as the GCY-18 warm temperature-responsive guanylyl cyclase thermoreceptor9 is transcriptionally upregulated in AFD upon a temperature upshift5,10. We find that as GCY-18 begins to accumulate at the AFD sensory endings, the GCY-23 cooler temperature-responsive thermoreceptor9 exhibits altered subcellular localization and increased retrograde trafficking, thereby increasing the functional GCY-18 to GCY-23 ratio in the AFD sensory compartment. Altered GCY-23 localization and trafficking requires PYT-1-dependent endocytosis, and we show that PYT-1-mediated modulation of the GCY-18 to GCY-23 protein ratio at the AFD sensory endings is necessary to shift the AFD response threshold towards warmer values following the temperature upshift. Our results describe a mechanism by which transcriptional and posttranscriptional mechanisms are temporally coordinated across sensory receptors to fine tune experience-dependent plasticity in the response of a single sensory neuron type.

neuroscience↗

bioRxiv2025

Pervasive and programmed nucleosome distortion patterns on single mammalian chromatin fibers

We present a genome-scale method to map the single-molecule co-occupancy of structurally distinct nucleosomes, subnucleosomes, and other protein-DNA interactions via long-read high-resolution adenine methyltransferase footprinting. Iteratively Defined Lengths of Inaccessibility (IDLI) classifies nucleosomes on the basis of shared patterns of intranucleosomal accessibility, into: i.) minimally-accessible chromatosomes; ii.) octasomes with stereotyped DNA accessibility from superhelical locations (SHLs) {+/-}1 through {+/-}7; iii.) highly-accessible unwrapped nucleosomes; and iv.) subnucleosomal species, such as hexasomes, tetrasomes, and other short DNA protections. Applying IDLI to mouse embryonic stem cell (mESC) chromatin, we discover widespread nucleosomal distortion on individual mammalian chromatin fibers, with >85% of nucleosomes surveyed displaying degrees of intranucleosomally accessible DNA. We observe epigenomic-domain-specific patterns of distorted nucleosome co-occupancy and positioning, including at enhancers, promoters, and mouse satellite repeat sequences. Nucleosome distortion is programmed by the presence of bound transcription factors (TFs) at cognate motifs; occupied TF binding sites are differentially decorated by distorted nucleosomes compared to unbound sites, and degradation experiments establish direct roles for TFs in structuring binding-site proximal nucleosomes. Finally, we apply IDLI in the context of primary mouse hepatocytes, observing evidence for pervasive nucleosomal distortion in vivo. Further genetic experiments reveal a role for the hepatocyte master regulator FOXA2 in directly impacting nucleosome distortion at hepatocyte-specific regulatory elements in vivo. Our work suggests extreme--but regulated--plasticity in nucleosomal DNA accessibility at the single-molecule level. Further, our study offers an essential new framework to model transcription factor binding, nucleosome remodeling, and cell-type specific gene regulation across biological contexts.

genomics↗

bioRxiv2024

AI-readiness for Biomedical Data: Bridge2AI Recommendations

Biomedical research is rapidly adopting artificial intelligence (AI). Yet the inherent complexity of biomedical data preparation requires implementing actionable, robust criteria for ethical and explainable AI (XAI) at the "pre-model" stage, encompassing data acquisition, detailed transformations, and ethical governance. Simple conformance to FAIR (Findable, Accessible, Interoperable, Reusable) Principles is insufficient. Here, we define criteria and practices for reliable AI-readiness of biomedical data, developed by the NIH Bridge to Artificial Intelligence (Bridge2AI) Standards Working Group across seven core dimensions of dataset AI-readiness: FAIRness, Provenance, Characterization, Ethics, Pre-model Explainability, Sustainability, and Computability. Conformance to these criteria provides a basis for pre-model scientific rigor and ethical integrity, mitigating downstream risks of bias and error prior to AI modeling. We apply and evaluate these standards across all four Bridge2AI flagship datasets, spanning functional genomics to clinical medicine, and encode them in machine-actionable metadata bound to the datasets. This framework sets a benchmark for preparing ethical, reusable datasets in biomedical AI and provides standardized methods for reliable pre-model data evaluation.

bioinformatics↗

bioRxiv2024

Divergent cytokine and transcriptional signatures control functional T follicular helper cell heterogeneity

Adaptive immune responses protect against multiple classes of pathogens, including viral, bacterial, fungal, and helminth infections. In all these settings, CD4+ T follicular helper (Tfh) cells tailor high-affinity class-switched B cells responses. How Tfh lineage sovereignty is established while allowing for this context-specific functional heterogeneity is unclear. Here, we identify Tfh transcriptional networks in response to diverse infections. While Bcl-6 is the transcriptional linchpin of the core Tfh signature, this is overlayed with pathogen-specific transcriptional modules that shape Tfh function. Cytokine-transcriptional Tfh programing in mouse and human lymphoid tissue demonstrated that type I interferon and TGF{beta} signaling direct individual Tfh subpopulations to instruct B cell output. Here, we provide a transcriptional map and cell surface resource to interrogate Tfh diversity in humans and mice. This resource can be leveraged to further understand the origins of immune flexibility, perform immune monitoring in infection and antibody-mediated diseases and to develop context-specific vaccines. ONE-SENTENCE SUMMARYDalit, Tan and colleagues provide a resource that functionally and transcriptionally profiles T follicular helper cells (Tfh) during diverse pathogen responses to reveal a blueprint for transcriptional flexibility and new tools to interrogate Tfh heterogeneity in mice and humans.

immunology↗

bioRxiv2024

Holding glycolysis in check though Alox15 activity is required for macrophage M2 commitment and function in tissue repair and anti-helminth immunity.

Macrophage polarization by type-2 cytokines is central to anti-helminth immunity and tissue repair. While some hallmark changes in macrophages are well-characterized and associated with protection against helminths, it is still unclear how macrophages exert their anti-helminth effects. In this context, we investigated Arachidonate 15-lipoxygenase (Alox15), a lipoxygenase well known for its role in macrophage polarization in the context of metabolic diseases, and a hallmark of type-2 macrophage (M2) human polarization. We show that in the absence of Alox15, M2 cannot trap and kill helminths. Surprisingly, expression of M2 markers was normal despite a loss of function. Instead, we found a concomitant increase in pro-inflammatory responses due to an uncontrolled activation of glycolysis. We further show that activation of Peroxisome proliferator-activated receptor-delta (PPAR-{delta}) by lipids downstream of Docosapentaenoic acid (DPA) can restore normal glycolysis control, highlighting a novel role for lipids in the fine-tuning of the metabolic support required for optimal macrophage polarization.

immunology↗

bioRxiv2023

B cell-stromal cell cross talk drives mesenteric lymph node eosinophilia during intestinal helminth infection

Eosinophils are involved in host protection against multicellular organisms including helminths and often participate in regulating long-lasting humoral responses. However, their recruitment to the gut-draining mesenteric lymph node (mLN), where they support the development of the adaptive immune response is still elusive. Here, we demonstrate the mechanism underlying the recruitment of eosinophils to the murine mLN post gastrointestinal helminth infection. We found that mLN eosinophils accumulated at immune interactive sites such as the interfollicular and paracortical regions in an IL-4R-dependent manner and was directly associated with the reduced availability of stromal derived eosinophil chemoattractants. Using multiplex imaging we confirmed that eosinophils associate within a stromal niche containing Lyve1+ lymphatic vessels, ER-TR7+Pdpn+ FRCs, and extrafollicular CD138+ plasma cells. Experiments utilising complete and mixed bone marrow chimeras demonstrated that mice lacking IL-4R expression or LT{beta} expression selectively on B cells had diminished eosinophilia and reduced extrafollicular plasma cell numbers within the mLN. When co-cultured with LT{beta}R activated FRCs, eosinophils gained an active phenotype with enhanced Il1rl1 (ST2) receptor expression. LT{beta}R ligation on FRCs resulted in enhanced IL-33 expression along with enrichment of distinct reactomes. Additionally, deletion of LT{beta}R in FRCs reduced the homing capability of eosinophils to the mLN, confirming the significance of lymphotoxin signalling in granulocyte recruitment. Overall, these results highlight the previously unknown role of B cell-stromal cell crosstalk in driving mLN eosinophilia and their potential role in regulating the quality and magnitude of the humoral immune response generated within the mLN.

immunology↗

bioRxiv2023

Helminth infection driven gastrointestinal hypermotility is independent of eosinophils and mediated by alterations in smooth muscle instead of enteric neurons

Intestinal helminth infection triggers a type 2 immune response that promotes a weep-and sweep response characterised by increased mucus secretion and intestinal hypermotility, which function to dislodge the worm from its intestinal habitat. Recent studies have discovered that several other pathogens cause intestinal dysmotility through major alterations to the immune and enteric nervous systems (ENS), and their interactions, within the gastrointestinal tract. However, the involvement of these systems has not been investigated for helminth infections. Eosinophils represent a key cell type recruited by the type 2 immune response and alter intestinal motility under steady-state conditions. Our study aimed to investigate whether intestinal dysmotility driven by murine hookworm, Nippostrongylus brasiliensis, infection involves eosinophils and how the ENS and smooth muscles of the gut are impacted. Eosinophil deficiency did not influence helminth-induced intestinal hypermotility and hypermotility did not involve gross structural or functional changes to the ENS. Hypermotility was instead associated with a dramatic increase in smooth muscle thickness and contractility. In summary our data indicate that, in contrast to other pathogens, helminth-induced intestinal hypermotility is driven by largely by myogenic, rather than neurogenic, alterations with such changes occurring independently of eosinophils. (<300 words) Author SummaryIntestinal helminth infection is a global threat to those living in poverty without adequate sanitation. Expulsion of intestinal worms is driven by a host type 2 immune response, characterised by increased eosinophils, that results in the intestinal hypermotility and mucus secretion that dislodge the worm from its luminal habitat. Intestinal motility is largely controlled by the local enteric nervous system (ENS) and can be regulated by close interactions between neurons and intestinal immune cells. Utilising Nippostrongylus brasiliensis as a model of murine hookworm infection, we investigated the contribution of the ENS and eosinophils to intestinal hypermotility and worm expulsion. Despite the critical role of the ENS in regulating typical intestinal function, very little alteration to ENS structure or function was observed following N. brasiliensis infection. Instead, infected animals displayed dramatically increased smooth muscle thickness and contractile strength. Neither helminth-induced intestinal hypermotility nor altered smooth muscle morphology required eosinophils. Our findings reveal that, in contrast to other intestinal pathogens, myogenic rather than neurogenic alterations drive small intestinal hypermotility and pathogen expulsion following hookworm infection. (<200 words)

immunology↗

bioRxiv2023

Molecular encoding of stimulus features in a single sensory neuron type enables neuronal and behavioral plasticity

Neurons modify their transcriptomes in response to an animals experience. How specific experiences are transduced to modulate gene expression and precisely tune neuronal functions are not fully defined. Here, we describe the molecular profile of a thermosensory neuron pair in C. elegans experiencing different temperature stimuli. We find that distinct salient features of the temperature stimulus including its duration, magnitude of change, and absolute value are encoded in the gene expression program in this single neuron, and identify a novel transmembrane protein and a transcription factor whose specific transcriptional dynamics are essential to drive neuronal, behavioral, and developmental plasticity. Expression changes are driven by broadly expressed activity-dependent transcription factors and corresponding cis-regulatory elements that nevertheless direct neuron- and stimulus-specific gene expression programs. Our results indicate that coupling of defined stimulus characteristics to the gene regulatory logic in individual specialized neuron types can customize neuronal properties to drive precise behavioral adaptation.

neuroscience↗

bioRxiv2022

Neuronal temperature perception induces specific defenses that enable C. elegans to cope with the enhanced reactivity of hydrogen peroxide at high temperature

Hydrogen peroxide is the most common reactive chemical that organisms face on the microbial battlefield. The rate with which hydrogen peroxide damages biomolecules required for life increases with temperature, yet little is known about how organisms cope with this temperature-dependent threat. Here, we show that Caenorhabditis elegans nematodes use temperature information perceived by sensory neurons to cope with the temperature-dependent threat of hydrogen peroxide produced by the pathogenic bacterium Enterococcus faecium. These nematodes preemptively induce the expression of specific hydrogen peroxide defenses in response to perception of high temperature by a pair of sensory neurons. These neurons communicate temperature information to target tissues expressing those defenses via an insulin/IGF1 hormone. This strategy, which we call "enhancer sensing," is the first example of a multicellular organism inducing their defenses to a chemical when they sense an inherent enhancer of the reactivity of that chemical.

neuroscience↗

bioRxiv2021

Cell-type specific induction of cyclo-oxygenase-2 in layer II/III prefrontal cortical neurons mediates stress-induced anxiety phenotypes in mice.

The ability of the medial prefrontal cortex (mPFC) to exert top-down control of behavior is affected by stress. The molecular response of mPFC to stress is incompletely understood, however, in part because of the regions cellular heterogeneity. Here we used single nucleus RNA sequencing (snRNAseq) to map specific molecular cell types within the mPFC and to detect cell-type specific transcriptional changes to foot-shock stress. We identified Ptgs2, encoding cyclo-oxygenase 2, as an important candidate that is upregulated in layer II/III excitatory neurons after stress. Specifically, Ptgs2 was transiently upregulated with shock-induced fear learning and fear expression, along with Bdnf, Nptx2, and Lingo1, in a layer II/III neuronal population marked by the neuronal excitatory gene Slc17a7 and cell-type specific neuropeptide Penk. These dynamic cell-type specific expression patterns identified with snRNAseq were validated with quantitative fluorescent in situ hybridization. Using a pharmacological approach, we found that systemic lumiracoxib, a selective Ptgs2-inhibitor, led to a significant reduction in fear expression. Furthermore, genetic ablation of Ptgs2 in excitatory Camk2a-expressing neurons led to reduced stress-induced anxiety-like behaviors. Together these findings suggest that Ptgs2 is expressed in a dynamic, cell-type specific way in Layer II/III Penk+ neurons in mPFC, and that its role in prostaglandin and /or endocannabinoid regulation within these neurons may be an important mediator of stress-related behavior.

neuroscience↗

bioRxiv2020

Feeding state functionally reconfigures a sensory circuit to drive thermosensory behavioral plasticity

Internal state alters sensory behaviors to optimize survival strategies. The neuronal mechanisms underlying hunger-dependent behavioral plasticity are not fully characterized. Here we show that feeding state regulates C. elegans negative thermotaxis behavior by engaging a modulatory circuit whose activity gates the output of the core thermotaxis network. Feeding state does not alter the activity of the core thermotaxis circuit comprised of AFD thermosensory and AIY interneurons. Instead, prolonged food deprivation potentiates temperature responses in the AWC sensory neurons, which inhibit the postsynaptic AIA interneurons to override and disrupt AFD-driven thermotaxis behavior. Acute inhibition and activation of AWC and AIA, respectively, restores negative thermotaxis in starved animals. We find that state-dependent modulation of AWC-AIA temperature responses requires INS-1 insulin-like peptide signaling from the gut and DAF-16 FOXO function in AWC. Our results describe a mechanism by which functional reconfiguration of a sensory network via gut-brain signaling drives state-dependent behavioral flexibility.

neuroscience↗

bioRxiv2020

Docosahexaenoic acid has stem cell-specific effects in the SVZ and restores olfactory neurogenesis and function in the aging brain

Fatty acids are well known as important constituents for the synthesis of membrane lipids and as sources of cellular energy in the CNS. However, fatty acids can also act as vital second messenger molecules in the nervous system and regulate the activity of many proteins affecting cell growth and survival. Here, we show that an essential dietary fatty acid, Decosahexaenoic acid, (DHA), can enhance stem cell function in vitro and in vivo. We found that this effect is not due to an increase in the overall proliferation rate of all neural progenitors, but is due to an increase in the number of multipotent stem cells that leads to greater levels of subventricular zone (SVZ) neurogenesis with restoration of olfactory function in aged mice. These effects were likely mediated through increased EGF-receptor sensitivity, a conversion of EGRFR+ progenitors back into an EGRFR+/GFAP+ stem cell state, and the activation of the PI3K/AKT signaling pathway, which is a critical pathway in many NSC cell functions including cell growth and survival. Together these data demonstrate that neural stem cells in the aged and quiescent neurogenic niche of the mouse SVZ retain their ability to self-renew and contribute to neurogenesis when apparently rejuvenated by DHA and PI3K/AKT pathway activation. DHA stimulation of this signaling enhances the number of multipotent stem cells and neurogenesis in young and aged rodent and human stem cells and hence may have implications for the manipulation of neural stem cells for brain repair. Significance StatementWe have identified potentially important effects of DHA on the stem cell population which may be unique to the SVZ stem cell niche. Our studies demonstrate that DHA can promote the production of neural stem cells, possibly via a non-proliferative mechanism stimulated by EGF receptor activation, and prolongs their viability. Aging animals undergo an apparent loss in SVZ stem cells and an associated decline in olfactory bulb function. We find that dietary DHA supplementation at least partially restores stem cell numbers, olfactory bulb neurogenesis and olfactory discrimination and memory in aged mice, demonstrating a capacity for rejuvenation is retained despite age-related changes to the niche, which has significant implications for ameliorating cognitive decline in aging and for endogenous brain repair.

neuroscience↗

bioRxiv2019

Infection with a small intestinal helminth Heligmosomoides polygyrus bakeri consistently alters microbial communities throughout the small and large intestine

Increasing evidence suggests that intestinal helminth infection can alter intestinal microbial communities with important impacts on the mammalian host. However, all of the studies to date utilize different techniques to study the microbiome and access different sites of the intestine with little consistency noted between studies. In the present study, we set out to perform a comprehensive analysis of the impact of intestinal helminth infection on the mammalian intestinal bacterial microbiome. For this purpose, we investigated the impact of experimental infection using the natural murine small intestinal helminth, Heligmosomoides polygyrus bakeri (Hpb) and examined possible alterations in both the mucous and luminal bacterial communities along the entire small and large intestine. We also explored the impact of common experimental variables, including the parasite batch and pre-infection microbiome, on the outcome of helminth-bacterial interactions. This work provides evidence that helminth infection reproducibly alters intestinal microbial communities - with an impact of infection noted along the entire length of the intestine. Although the exact nature of helminth-induced alterations to the intestinal microbiome differed depending on the parasite batch and microbiome community structure present prior to infection, changes extended well beyond the introduction of new bacterial species by the infecting larvae. Moreover, striking similarities between different experiments were noted, including the consistent outgrowth of a bacterium belonging to the Peptostreptococcaceae family throughout the intestine.\n\nAuthor SummaryIncreasing evidence indicates a role for interactions between intestinal helminths and the microbiome in regulating mammalian health, and a greater understanding of helminth-microbiota interactions may open the path for the development of novel immunomodulatory therapies. However, such studies are hampered by the inconsistent nature of the data reported so far. Such inconsistancies likely result from variations in the experimental and technological methodologies employed to investigate helminth-microbiota interactions and well has natural variation in the starting microbiome composition and/or worm genetics. We conducted a thorough study in which the reproducibility of helminth-induced alterations of microbial communities was determined and impact of common experimental variables - such as the starting microbiome and parasite batch - was determined. Our work reveals the robust ability of small intestinal helminth infection to alter microbial communities along the entire length of the intestine and additionally identifies a single bacterium that is strongly associated with infection across multiple experiments.

microbiology↗

bioRxiv2019

Apollo: Democratizing genome annotation

Genome annotation is the process of identifying the location and function of a genomes encoded features. Improving the biological accuracy of annotation is a complex and iterative process requiring researchers to review and incorporate multiple sources of information such as transcriptome alignments, predictive models based on sequence profiles, and comparisons to features found in related organisms. Because rapidly decreasing costs are enabling an ever-growing number of scientists to incorporate sequencing as a routine laboratory technique, there is widespread demand for tools that can assist in the deliberative analytical review of genomic information. To this end, Apollo is an open source software package that enables researchers to efficiently inspect and refine the precise structure and role of genomic features in a graphical browser-based platform.\n\nIn this paper we first outline some of Apollos newer user interface features, which were driven by the needs of this expanding genomics community. These include support for real-time collaboration, allowing distributed users to simultaneously edit the same encoded features while also instantly seeing the updates made by other researchers on the same region in a manner similar to Google Docs. Its technical architecture enables Apollo to be integrated into multiple existing genomic analysis pipelines and heterogeneous laboratory workflow platforms. Finally, we consider the implications that Apollo and related applications may have on how the results of genome research are published and made accessible. O_LISource: https://github.com/GMOD/Apollo\nC_LIO_LILicense (BSD-3): https://github.com/GMOD/Apollo/blob/master/LICENSE.md\nC_LIO_LIDocker: https://hub.docker.com/r/gmod/apollo/tags/, https://github.com/GMOD/docker-apollo\nC_LIO_LIRequirements: JDK 1.8, Node v6.0+\nC_LIO_LIUser guide: http://genomearchitect.org; technical guide: http://genomearchitect.readthedocs.io/en/latest/\nC_LIO_LIMailing list: apollo@lists.lbl.gov\nC_LI

bioinformatics↗

bioRxiv2017

The Parasite Extinction Assessment & Red List: an open-source, online biodiversity database for neglected symbionts

Parasite conservation is a rapidly growing field at the intersection of ecology, epidemiology, parasitology, and public health. The overwhelming diversity of parasitic life on earth, and recent work showing that parasites and other symbionts face severe extinction risk, necessitates infrastructure for parasite conservation assessments. Here, we describe the release of the Parasite Extinction Assessment & Red List (PEARL) version 1.0, an open-access database of conservation assessments and distributional data for almost 500 macroparasitic invertebrates. The current approach to vulnerability assessment is based on range shifts and loss from climate change, and will be expanded as additional data (e.g., host-parasite associations and coextinction risk) is consolidated in PEARL. The web architecture is also open-source, scalable, and extensible, making PEARL a template for more eZcient red listing for other high-diversity, data-de1cient groups. Future iterations will also include new functionality, including a user-friendly open data pository and automated assessment and re-listing.

ecology↗