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78 results for “Pathogen evolution”
ROS and SGI data for manuscript "The perception and evolution of flagellin, cold shock protein, and elongation factor Tu from vector-borne bacterial plant pathogens"
<p>This contains raw data for the ROS and seedling growth inhibition (SGI) assays collected for the manuscript "The perception and evolution of flagellin, cold shock protein, and elongation factor Tu from vector-borne bacterial plant pathogens". For a quick reference, there are two spreadsheets listing all the Max RLUs and Z-scores for the experiments, but the actual output of each plate reader is also included. </p>
Data from: Inferring epidemiologic dynamics from viral evolution: 2014–2015 Eurasian/North American highly pathogenic avian influenza viruses exceed transmission threshold, R0 = 1, in wild birds and poultry in North America
Highly pathogenic avian influenza virus (HPAIV) is a multi-host pathogen with lineages that pose health risks for domestic birds, wild birds, and humans. One mechanism of intercontinental HPAIV spread is through wild bird reservoirs and wild birds were the likely sources of a Eurasian (EA) lineage HPAIV into North America in 2014. The introduction resulted in several reassortment events with North American (NA) lineage low pathogenic avian influenza viruses and the reassortant EA/NA H5N2 went on to cause one of the largest HPAIV poultry outbreaks in North America. We evaluated three hypotheses about novel HPAIV introduced into wild and domestic bird hosts: (i) transmission of novel HPAIVs in wild birds was restricted by mechanisms associated with highly-pathogenic phenotypes; (ii) the HPAIV poultry outbreak was not self-sustaining and required viral input from wild birds; (iii) reassortment of the EA H5N8 generated reassortant EA/NA AIVs with a fitness advantage over fully Eurasian lineages in North American wild birds. We used a time-rooted phylodynamic model that explicitly incorporated viral population dynamics with evolutionary dynamics to estimate the basic reproductive number (R0) and viral migration among host types in domestic and wild birds, as well as between the EA H5N8 and EA/NA H5N2 in wild birds. We did not find evidence to support hypothesis (i) or (ii) as our estimates of the transmission parameters suggested that the HPAIV outbreak met or exceeded the threshold for persistence in wild birds (R0 > 1) and poultry (R0 ≈ 1) with minimal estimated transmission among host types. There was also no evidence to support hypothesis (iii) because R0 values were similar among EA H5N8 and EA/NA H5N2 in wild birds. Our results suggest that this novel HPAIV and reassortments did not encounter any transmission barriers sufficient to prevent persistence when introduced to wild or domestic birds.
Data from: Ultrafast evolution and loss of CRISPRs following a host shift in a novel wildlife pathogen, Mycoplasma gallisepticum
Measureable rates of genome evolution are well documented in human pathogens but are less well understood in bacterial pathogens in the wild, particularly during and after host switches. Mycoplasma gallisepticum (MG) is a pathogenic bacterium that has evolved predominantly in poultry and recently jumped to wild house finches (Carpodacus mexicanus), a common North American songbird. For the first time we characterize the genome and measure rates of genome evolution in House Finch isolates of MG, as well as in poultry outgroups. Using whole genome sequences of 12 House Finch isolates across a 13-year serial sample and an additional four newly sequenced poultry strains, we estimate a nucleotide diversity in House Finch isolates of only ~2% of ancestral poultry strains and a nucleotide substitution rate of 0.8 – 1.2 X 10-5 per site per year both in poultry and in House Finches, an exceptionally fast rate rivaling some of the highest estimates reported thus far for bacteria. We also found high diversity and complete turnover of CRISPR arrays in poultry MG strains prior to the switch to the House Finch host, but after the invasion of House Finches, there is progressive loss of CRISPR repeat diversity, and recruitment of novel CRISPR repeats ceases. Recent (2007) House Finch MG strains retain only ~50% of the CRISPR repertoire founding (1994-95) strains and have lost the CRISPR-associated genes required for CRISPR function. Our results suggest that genome evolution in bacterial pathogens of wild birds can be extremely rapid and in this case is accompanied by apparent functional loss of CRISPRs.
Pleiotropy promotes the evolution of inducible immune responses in a model of host-pathogen coevolution
<p>The archives uploaded here include the code used to perform the evolutionary simulations as described in <em>Pleiotropy promotes the evolution of inducible immune responses in a model of host-pathogen coevolution </em>authors: Martin,R. Tate, A. as well as the data that was used in the generation of the figures for that paper. Code requires the Julia programming language and necessary packages to run.</p>
Dataset for "Population-level transposable element expression dynamics influence trait evolution in a fungal crop pathogen"
<p><strong>Supplementary Tables</strong></p> <p><strong>Supplementary Table S1: </strong>SRA accession list of RNAseq reads.</p> <p><strong>Supplementary Table S2:</strong> Genomic localization of TEs in gene elements and 10 kb windows upstream and downstream of the transcription start site (TSS) in the reference genome IPO323.</p> <p><strong>Supplementary Table S3:</strong> Genome-wide TE insertion polymorphism (TIPs) in the pathogen population. 0 represents TE absence and 1 represents TE presence.</p> <p><strong>Supplementary Table S4:</strong> Gene expression (log-transformed RPKM) values across the population.</p> <p><strong>Supplementary Table S5:</strong> Locus-specific transcript abundance at individual TE loci (FPKM) across individuals.</p> <p><strong>Supplementary Table S6:</strong> Percent of expressed copies within each TE family in the reference genome IPO323 and percent expressed TE copies in each TE family across the population.</p> <p><strong>Supplementary Table S7:</strong> Linkage disequilibrium of TIP in the genome and neighboring SNPs within the 600bp distance from the TE loci.</p> <p><strong>Supplementary Table S8:</strong> Genome-wide association mapping of the virulence-associated trait (PLACP: percent leaf area covered by pycnidia) and TE insertion polymorphisms in the genome.</p> <p><strong>Supplementary Table S9:</strong> TIPs in the genome significantly associated with metabolite peak intensity variation in the pathogen population (filtered by Bonferroni threshold).</p>
Supplementary Tables for "Population-level transposable element expression dynamics influence trait evolution in a fungal crop pathogen"
<p><strong>Supplementary Table S1:</strong> Genomic localization of TEs in gene elements and 10 kb windows upstream and downstream of the transcription start site (TSS) in the reference genome IPO323.</p><p><strong>Supplementary Table S2:</strong> Genome-wide TE insertion polymorphism (TIPs) in the pathogen population. 0 represents TE absence and 1 represents TE presence.</p><p><strong>Supplementary Table S3:</strong> Gene expression (log transformed RPKM) values across the population.</p><p><strong>Supplementary Table S4:</strong> Locus-specific transcript abundance at individual TE loci (FPKM) across individuals.</p><p><strong>Supplementary Table S5:</strong> Percent of expressed copies within each TE family in the reference genome IPO323 and percent expressed TE copies in each TE family across the population.</p><p><strong>Supplementary Table S6:</strong> Linkage disequilibrium of TIP in the genome and neighboring SNPs within the 600bp distance from the TE loci.</p><p><strong>Supplementary Table S7:</strong> Genome-wide association mapping of the virulence-associated trait (PLACP: percent leaf area covered by pycnidia) and TE insertion polymorphisms in the genome.</p><p><strong>Supplementary Table S8:</strong> metabolite peak variation in the pathogen population for individual isolates</p><p><strong>Supplementary Table S9:</strong> TIPs in the genome significantly associated with metabolite peak intensity variation in the pathogen population (filtered by Bonferroni threshold).</p><p><strong>Supplementary Table S10: </strong>SRA accession list of RNAseq reads.</p>
Data from: Trade-offs and evolution of thermal adaptation in the Irish potato famine pathogen Phytophthora infestans
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Data from: Inferring epidemiologic dynamics from viral evolution: 2014–2015 Eurasian/North American highly pathogenic avian influenza viruses exceed transmission threshold, R0 = 1, in wild birds and poultry in North America
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Data from: Evolution of Drosophila resistance against different pathogens and infection routes entails no detectable maintenance costs
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Data from: Ultrafast evolution and loss of CRISPRs following a host shift in a novel wildlife pathogen, Mycoplasma gallisepticum
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Data from: Evolution of both host resistance and tolerance to an emerging bacterial pathogen
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Data from: Ancestral chytrid pathogen remains hypervirulent following its long co-evolution with amphibian hosts
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Data from: Mitotic recombination and rapid genome evolution in the invasive forest pathogen Phytophthora ramorumm
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Data from: Evolution of increased virulence is associated with decreased spite in the insect-pathogenic bacterium Xenorhabdus nematophila
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Data from: Contrasting evolution of virulence and replication rate in an emerging bacterial pathogen
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Pathogen defence is a potential driver of social evolution in ambrosia beetles
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Data from: Immune priming specificity within and across generations reveals the range of pathogens affecting evolution of immunity in an insect
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Data from: Microbe-mediated host defence drives the evolution of reduced pathogen virulence
Microbes that protect their hosts from pathogens are widespread in nature and are attractive disease control agents. Given that pathogen adaptation to barriers against infection can drive changes in pathogen virulence, 'defensive microbes' may shape disease severity. Here we show that co-evolving a microbe with host-protective properties (Enterococcus faecalis) and a pathogen (Staphylococcus aureus) within Caenorhabditis elegans hosts drives the evolution of reduced pathogen virulence as a by-product of adaptation to the defensive microbe. Using both genomic and phenotypic analyses, we discover that the production of fewer iron-scavenging siderophores by the pathogen reduces the fitness of the defensive microbe and underpins the decline in pathogen virulence. These data show that defensive microbes can shape the evolution of pathogen virulence and that the mechanism of pathogen resistance can determine the direction of virulence evolution.
Data from: The role of the environment in the evolution of tolerance and resistance to a pathogen
Defense against parasites can be divided into resistance, which limits parasite burden, and tolerance, which reduces pathogenesis at a given parasite burden. Distinguishing between the two and understanding which defense is favored by evolution in different ecological settings are important, as they lead to fundamentally different evolutionary trajectories of host-parasite interactions. We let the mosquito Aedes aegypti evolve under different food levels and with either no parasite, a constant parasite, or a coevolving parasite (the microsporidian Vavraia culicis). We then tested tolerance and resistance of the evolved lines on a population level at the two food levels. Exposure to parasites during evolution increased resistance and tolerance, but there were no differences between the lines evolved with coevolving or constant parasites. Mosquitoes that had evolved with food restriction had higher resistance than those evolved with high food but similar tolerance. The mosquitoes that had restricted food when being tested had lower tolerance than those with normal food, but there was no difference in resistance. Our results emphasize the complexity and dependence on environmental conditions of the evolution and expression of resistance and tolerance and help to evaluate some of the predictions about the evolution of host defense against parasites.
Data from: Evolution of pathogenicity traits in the apple scab fungal pathogen in response to the domestication of its host
Understanding how pathogens emerge is essential to bring disease-causing agents under durable human control. Here, we used cross-pathogenicity tests to investigate changes in life history traits of the fungal pathogen Venturia inaequalis associated with host-tracking during the domestication of apple and subsequent host range expansion on the wild European crabapple (Malus sylvestris). Pathogenicity of 40 isolates collected in wild and domesticated ecosystems were assessed on the domesticated apple, its central Asian main progenitor (M. sieversii) and M. sylvestris. Isolates from wild habitats in the centre of origin of the crop were not pathogenic on the domesticated apple and less aggressive than other isolates on their host of origin. Isolates from the agro-ecosystem in central Asia infected a higher proportion of plants with higher aggressiveness, on both the domesticated host and its progenitor. Isolates from the European crabapple were still able to cause disease on other species but were less aggressive and less frequently virulent on these hosts than their endemic populations. Our results suggest that the domestication of apple was associated with the acquisition of virulences in the pathogen following host-tracking. The spread of the disease in the agro-ecosystem would also have been accompanied by an increase in overall pathogenicity.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.