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78 results for “Pathogen evolution”
A chromosome-level genome resource for studying virulence mechanisms and evolution of the coffee rust pathogen Hemileia vastatrix
<p>Recurrent epidemics of coffee leaf rust, caused by the fungal pathogen <em>Hemileia vastatrix,</em> have constrained the sustainable production of Arabica coffee for over 150 years. The ability of <em>H. vastatrix </em>to overcome resistance in coffee cultivars and evolve new races is inexplicable for a pathogen that supposedly only utilizes clonal reproduction. Understanding the evolutionary complexity between <em>H. vastatrix</em> and its only known host, including determining how the pathogen evolves virulence so rapidly is crucial for disease management. Achieving such goals relies on the availability of a comprehensive and high-quality genome reference assembly. To date, two reference genomes have been assembled and published for <em>H. vastatrix</em> that, while useful, remain fragmented and do not represent chromosomal scaffolds. Here, we present a complete scaffolded pseudochromosome-level genome resource for <em>H. vastatrix </em>strain 178a (Hv178a). Our initial assembly revealed an unusually high degree of gene duplication (over 50% BUSCO basidiomycota_odb10 genes). Upon inspection, this was predominantly due to a single scaffold that itself showed 91.9% BUSCO Completeness. Taxonomic analysis of predicted BUSCO genes placed this scaffold in Exobasidiomycetes and suggests it is a distinct genome, which we have named Hv178a associated fungal genome (Hv178a AFG). The high depth of coverage and close association with Hv178a raises the prospect of symbiosis, although we cannot completely rule out contamination at this time. The main Ca. 546 Mbp Hv178a genome was primarily (97.7%) localised to 11 pseudochromosomes (51.5 Mb N50), building the foundation for future advanced studies of genome structure and organization. Citation: https://doi.org/10.1101/2022.07.29.502101</p>
Implications of the three-dimensional chromatin organization for genome evolution in a fungal plant pathogen
<p><span>The spatial organization of eukaryotic genomes is linked to their biological functions, although it is not clear how this impacts the overall evolution of a genome. Here, we uncover the three-dimensional (3D) genome organization of the phytopathogen <em>Verticillium dahliae</em>,<em> </em>known to possess distinct genomic regions, designated adaptive genomic regions (AGRs), enriched in transposable elements and genes that mediate host infection. Short-range DNA interactions form clear topologically associating domains (TADs) with gene-rich boundaries that show reduced levels of gene expression and reduced genomic variation. Intriguingly, TADs are less clearly insulated in AGRs than in the core genome. At a global scale, the genome contains bipartite long-range interactions, particularly enriched for AGRs and more generally containing segmental duplications. Notably, the patterns observed for <em>V. dahliae </em>are also present in other <em>Verticillium</em> species. Thus, our analysis links 3D genome organization to evolutionary features conserved throughout the <em>Verticillium</em> genus.</span></p>
The effect of a temperature‐sensitive prophage on the evolution of virulence in an opportunistic bacterial pathogen
<p>Viruses are key actors of ecosystems and have major impacts on global biogeochemical cycles. Prophages deserve particular attention as they are ubiquitous in bacterial genomes and can enter a lytic cycle when triggered by environmental conditions. We explored how temperature affects the interactions between prophages and other biological levels by using an opportunistic pathogen, the bacterium <em>Serratia marcescens</em>, that harbours several prophages and that had undergone an evolution experiment under several temperature regimes. We found that the release of one of the prophages was temperature-sensitive and malleable to evolutionary changes. We further discovered that the virulence of the bacterium in an insect model also evolved and was positively correlated with phage release rates. We determined through analysis of genetic and epigenetic data that changes in the bacterial outer cell wall structure possibly explain this phenomenon. We hypothezise that the temperature-dependent phage release rate acted as a selection pressure on <em>S. marcescens</em> and that it resulted in modified bacterial virulence in the insect host. Our study system illustrates how viruses can mediate the influence of abiotic environmental changes to other biological levels and thus be involved in ecosystem feedback loops.</p>
Reference data from the Pathomove simulation, for the manuscript "Novel pathogen introduction triggers rapid evolution in animal social movement strategies"
<p>This is a reference dataset of multiple runs of the 'Pathomove' simulation, to accompany the manuscript "Novel pathogen introduction rapidly alters the evolution of movement, restructuring animal societies". The datasets are in the form of R data objects saved as Rds files.</p> <p>This version of the data is intended to accompany a resubmission to <em>eLife</em>.</p>
The effect of a temperature‐sensitive prophage on the evolution of virulence in an opportunistic bacterial pathogen
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Data from: Experimental evolution of insect immune memory versus pathogen resistance
Under strong pathogen pressure, insects often evolve resistance to infection. Many insects are also protected via immune memory ('immune priming'), whereby sub-lethal exposure to a pathogen enhances survival after secondary infection. Theory predicts that immune memory should evolve when the pathogen is highly virulent, or when pathogen exposure is relatively rare. However, there are no empirical tests of these hypotheses, and the adaptive benefits of immune memory relative to direct resistance against a pathogen are poorly understood. To determine the selective pressures and ecological conditions that shape immune evolution, we imposed strong pathogen selection on flour beetle (Tribolium castaneum) populations, infecting them with Bacillus thuringiensis (Bt) for 11 generations. Populations injected first with heat-killed and then live Bt each generation evolved high basal resistance against multiple Bt strains. In contrast, populations injected only with a high dose of live Bt evolved a less effective but strain-specific priming response. Control populations injected with heat-killed Bt did not evolve priming; and in the ancestor, priming was effective only against a low Bt dose. Intriguingly, one replicate population first evolved priming and subsequently evolved basal resistance, suggesting the potential for dynamic evolution of different immune strategies. Our work is the first report showing that pathogens can select for rapid modulation of insect priming ability, allowing hosts to evolve divergent immune strategies (generalized resistance vs. specific immune memory) with potentially distinct mechanisms.
Data from: Incomplete host immunity favors the evolution of virulence in an emergent pathogen
Immune memory evolved to protect hosts from reinfection, but incomplete responses that allow future reinfection might inadvertently select for more harmful pathogens. We present empirical and modeling evidence that incomplete immunity promotes the evolution of higher virulence in a natural host-pathogen system. We performed sequential infections of house finches with Mycoplasma gallisepticum strains of varying virulence. Virulent bacterial strains generated stronger host protection against reinfection than less virulent strains, and thus excluded less virulent strains from infecting previously-exposed hosts. In a two-strain model, the resulting fitness advantage selected for an almost two-fold increase in pathogen virulence. Thus, the same immune systems that protect hosts from infection can concomitantly drive the evolution of more harmful pathogens in nature.
Evolution of sympatric host-specialized lineages of the fungal plant pathogen Zymoseptoria passerinii in natural ecosystems
<p>This repository contains the data sets from the research paper "Evolution of sympatric host-specialized lineages of the fungal plant pathogen <em>Zymoseptoria passerinii</em> in natural ecosystems"</p>
Comparative genomics reveals evolution traits, mating strategies and pathogenicity-related genes variation of Botryosphaeriaceae
<p><em>Botryosphaeriaceae</em>, as a major family of the largest class of kingdom fungi <em>Dothideomycetes</em>, encompasses phytopathogens, saprobes, and endophytes. Many members of this family are opportunistic phytopathogens with a wide host range and worldwide geographical distribution, and can infect many economically important plants, including food crops and bio-material plants. To date, however, little is known about the family evolutionary characterization, mating strategies, and pathogenicity-related genes variation from a comparative genome perspective. Here, we conducted the first large-scale whole-genome comparison of 271 <em>Dothideomycetes</em>, including 19 species in <em>Botryosphaeriaceae</em>. The comparative genome analysis provided a clear classification of <em>Botryosphaeriaceae</em> in <em>Dothideomycetes</em> and indicated that <em>Botryosphaeriaceae</em> pathogenicity evolution undergoes multiple times. Mating strategies analysis demonstrated at least 3 transitions were found within <em>Botryosphaeriaceae</em> from heterothallism to homothallism. Additionally, pathogenicity-related genes contents in different species within <em>Botryosphaeriaceae</em> varied greatly, indicating that a secondary lineage expansion occurs in speciation. These findings cast new insights into evolution traits, mating strategies and pathogenicity-related genes variation of <em>Botryosphaeriaceae</em>.</p>
Complete telomere-to-telomere genomes uncover virulence evolution conferred by chromosome fusion in oomycete plant pathogens
<p><span>Variations in chromosome number are occasionally observed among oomycetes, a group that includes many plant pathogens, but the emergence of such variations and their effects on genome and virulence evolution remain ambiguous. We generated complete telomere-to-telomere genome assemblies for <em>Phytophthora sojae</em>, <em>Globisporangium ultimum</em>, <em>Pythium oligandrum</em>, and <em>G. spinosum</em>. Reconstructing the karyotype of the most recent common ancestor in Peronosporales revealed that frequent chromosome fusion and fission drove changes in chromosome number. Centromeres enriched with <em>Copia</em>-like transposons may contribute to chromosome fusion and fission events. Chromosome fusion facilitated the emergence of pathogenicity genes and their adaptive evolution. Effectors tended to duplicate in the sub-telomere regions of fused chromosomes, which exhibited evolutionary features distinct to the non-fused chromosomes. By integrating ancestral genomic dynamics and structural predictions, we have identified secreted Ankyrin repeat-containing proteins (ANKs) as a novel class of effectors in <em>P. sojae</em>. Phylogenetic analysis and experiments further revealed that ANK is a specifically expanded effector family in oomycetes. These results revealed chromosome dynamics in oomycete plant pathogens, and provided novel insights into karyotype and effector evolution.</span></p>
Pathogen non-planktonic phases within the urinary tract impact early infection and resistance evolution - Data
<p>This upload contains data that is necessary to re-create the figures for the manuscript "<strong>Infection dynamics in the urinary tract - The importance of non-planktonic phases during early infection and resistance evolution</strong>" by Raatz et al. published in The ISME Journal (<a href="https://doi.org/10.1093/ismejo/wrae191">https://doi.org/10.1093/ismejo/wrae191</a>).</p> <p>This manuscript is available as a bioRxiv preprint at https://www.biorxiv.org/content/10.1101/2023.10.23.563535.</p> <p>The related upload with DOI 10.5281/zenodo.10025282 contains the scripts to compute this data set, as well as the scripts for plotting.</p> <p> </p>
Supplementary Data for: Whole genome sequencing elucidates the species-wide diversity and evolution of fungicide resistance in the early blight pathogen Alternaria solani
<p>Supplementary Data for: Whole genome sequencing elucidates the species-wide diversity and evolution of fungicide resistance in the early blight pathogen Alternaria solani</p> <p>This repository contains:</p> <p>SNP call data / VCF file</p> <p>Scripts for all processing steps from mapping up to PCA and phylogenetic analyses (script.ts)<br> Scripts for population genomic analyses with LEA and PopGenome (scripts.SE)<br> All script names are self explanatory.</p>
Bacterial predation of a fungal wheat pathogen: Prelude to experimental evolution of enhanced biocontrol agents
<p><span>Research to identify appropriate biological agents for controlling pathogens might exploit experimental evolution to select for enhanced antagonism against pathogens. We report development of an experimental regime facilitating this approach featuring the broad-spectrum bacterial predator <em>Myxococcus</em> <em>xanthus</em> and the fungal wheat pathogen <em>Zymoseptoria</em> <em>tritici</em>. We demonstrate that <em>Z. tritici</em>, a major cause of crop loss and fungicide use worldwide, both fuels growth of and is killed by <em>M. xanthus</em> on wheat straw, a likely source of vernal seedling infection. <em>M. xanthus</em> is first found capable of density-dependent growth on moistened straw alone, unaided by <em>Z. tritici</em> as prey, growth that also depends on how long straw was moistened before <em>M. xanthus</em> inoculation. Such growth of non-cellulolytic myxobacteria on plant detritus may have implications for understanding their roles in nutrient cycling. However, straw with <em>Z. tritici </em>is found to fuel greater <em>M. xanthus </em>growth than straw alone under many conditions. After shorter moistening, growth by low-density <em>M. xanthus</em> populations is found to be fully dependent on <em>Z. tritici</em>. Such pathogen-dependent <em>M. xanthus</em> populations could be sustained with population replacement over five one-week growth cycles, indicating feasibility of conducting long-term experimental evolution with this system. Further, <em>M. xanthus</em> is found to kill majorities of <em>Z. tritici</em> populations on both buffered agar and straw. Our results suggest that myxobacteria may serve as effective biocontrol agents of <em>Z. tritici</em> and are amenable to long-term experimental selection for enhanced killing of this pathogen, an approach broadly applicable to many potential biocontrol agents and target pathogens.</span></p>
Data from: Incomplete host immunity favors the evolution of virulence in an emergent pathogen
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Bacterial predation of a fungal wheat pathogen: Prelude to experimental evolution of enhanced biocontrol agents
Open the record for dataset details and reuse information.
Data from: Experimental evolution of insect immune memory versus pathogen resistance
Open the record for dataset details and reuse information.
Data from: Contrasting evolution of virulence and replication rate in an emerging bacterial pathogen
Host resistance through immune clearance is predicted to favour pathogens that are able to transmit faster and are hence more virulent. Increasing pathogen virulence is, in turn, typically assumed to be mediated by increasing replication rates. However, experiments designed to test how pathogen virulence and replication rates evolve in response to increasing host resistance, as well as the relationship between the two, are rare and lacking for naturally-evolving host-pathogen interactions. We inoculated 55 isolates of Mycoplasma gallisepticum collected over 20 years from outbreak, into house finches (Haemorhous mexicanus) from disease-unexposed populations, which have not evolved protective immunity to M. gallisepticum. We show using three different metrics of virulence (body mass loss, symptom severity and putative mortality rate) that virulence has increased linearly over >150,000 bacterial generations since outbreak (1994-2015). By contrast, while replication rates increased from outbreak through to the initial spread of resistance (1994-2004), no further increases have occurred subsequently (2007-2015). Finally, as a consequence, we found that any potential mediating effect of replication rate on virulence evolution was restricted to the period when host resistance was initially increasing in the population. Taken together, our results show that pathogen virulence and replication rates can evolve independently, particularly after the initial spread of host resistance. We hypothesize that the evolution of pathogen virulence can be driven primarily by processes such as immune manipulation after resistance spreads in host populations.
Data from: Evolution of Drosophila resistance against different pathogens and infection routes entails no detectable maintenance costs
Pathogens exert a strong selective pressure on hosts, entailing host adaptation to infection. This adaptation often affects negatively other fitness-related traits. Such trade-offs may underlie the maintenance of genetic diversity for pathogen resistance. Trade-offs can be tested with experimental evolution of host populations adapting to parasites, using two approaches: (1) measuring changes in immunocompetence in relaxed-selection lines and (2) comparing life-history traits of evolved and control lines in pathogen-free environments. Here, we used both approaches to examine trade-offs in Drosophila melanogaster populations evolving for over 30 generations under infection with Drosophila C Virus or the bacterium Pseudomonas entomophila, the latter through different routes. We find that resistance is maintained after up to 30 generations of relaxed selection. Moreover, no differences in several classical life-history traits between control and evolved populations were found in pathogen-free environments, even under stresses such as desiccation, nutrient limitation, and high densities. Hence, we did not detect any maintenance costs associated with resistance to pathogens. We hypothesize that extremely high selection pressures commonly used lead to the disproportionate expression of costs relative to their actual occurrence in natural systems. Still, the maintenance of genetic variation for pathogen resistance calls for an explanation.
Pathogen defence is a potential driver of social evolution in ambrosia beetles
Social immunity – the collective behavioural defences against pathogens - is considered a crucial evolutionary force for the maintenance of insect societies. It has been described and investigated primarily in eusocial insects, but its role in the evolutionary trajectory from parental care to eusociality is little understood. Here, we report on the existence, plasticity, effectiveness and consequences of social pathogen defence in experimental nests of cooperatively breeding ambrosia beetles. After an Aspergillus-spore-buffer solution or a control buffer solution had been injected in laboratory nests, totipotent adult female workers increased their activity and hygienic behaviours like allogrooming and cannibalism. Such social immune responses had not been described for any non-eusocial, cooperatively breeding insect before. Removal of beetles from <i>Aspergillus</i>-treated nests in a paired experimental design revealed that the hygienic behaviours of beetles significantly reduced pathogen prevalence in the nest. Furthermore, in response to pathogen injections, female helpers delayed dispersal and thus prolonged their cooperative phase within their mother's nest. Our findings of appropriate social responses to an experimental immune challenge in a cooperatively breeding beetle corroborate the view that social immunity is not an exclusive attribute of eusocial insects, but rather a concomitant and presumably important feature in the evolutionary transitions towards complex social organization.
Assemblies for 'Mixed strain pathogen populations accelerate the evolution of antibiotic resistance in patients'
<p>Antibiotic resistance poses a global health threat, but the within-host drivers of resistance remain poorly understood. Pathogen populations are often assumed to be clonal within hosts, and resistance is thought to emerge due to selection for de novo variants. Here we show that mixed strain populations are common in the opportunistic pathogen <i>P. aeruginosa</i>. Crucially, resistance evolves rapidly in patients colonized by multiple strains through selection for pre-existing resistant strains. In contrast, resistance evolves sporadically in patients colonized by single strains due to selection for novel resistance mutations. However, strong trade-offs between resistance and growth rate occur in mixed strain populations, suggesting that within-host diversity can also drive the loss of resistance in the absence of antibiotic treatment. In summary, we show that the within-host diversity of pathogen populations plays a key role in shaping the emergence of resistance in response to treatment.</p>
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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.