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Phenotypic data related to genetic architecture of transmission stage production and virulence in schistosome parasites

These data were generated related to the study of the Genetic architecture of transmission stage production and virulence in schistosome parasites. Abstract: Both theory and experimental data from multiple pathogens suggest that the production of transmission stages should be strongly associated with virulence, but the genetic bases of parasite transmission/virulence traits are poorly understood. In the blood fluke Schistosoma mansoni, parasite genotypes show extensive variation in numbers of cercariae larvae shed from infected snails. Furthermore, high shedding parasites cause high mortality to snails while low shedding parasites cause low mortality, consistent with expected trade-offs between parasite transmission and virulence. To understand the genetic basis of transmission stage production/virulence, we conducted reciprocal crosses between schistosomes from two laboratory populations that differ 8-fold in cercarial shedding and in their virulence to inbred snail hosts. Each parasite generation, we determined four-week cercarial shedding profiles in inbred Biomphalaria glabrata snails infected with single parasite larvae. We sequenced the whole genome of the F0 parents and the exome of the F1 progeny and 188 F2 progeny from each cross, and used linkage mapping to reveal quantitative trait loci (QTLs) underlying transmission stage production. Cercarial production is polygenic: we found three major QTLs on chromosome 1, 3 and 5 (Log-of-the-odds (LOD) = 5.61, 8.19, 6.25) and two minor QTLs on chromosome 2 and 4. These QTLs act additively and explained 28.56% of the phenotypic variation in cercarial shedding. Alleles inherited from the high and low shedding parents were co-dominant at all QTLs, except for chr. 1 and chr. 4 where the “high cercarial shedding” allele is recessive. These results demonstrate that the genetic architecture of key traits directly relevant to schistosome ecology can be dissected using classical linkage mapping approaches, and set the stage for fine mapping and functional validation of the genes involved using the growing armory of functional and cell biology tools available for this parasite.   This dataset is made of 4 tables: <ul> <li>F0_parental_populations.csv</li> <li>F1.csv</li> <li>F2.csv</li> <li>sex.tsv</li> </ul>   F0_parental_populations.csv   This table contains the number of cercariae produced by each individual Biomphalaria glabrata Bg26 snails infected with single genotypes of Schistosoma mansoni parasite. We have compared the transmission stage production between two different populations of S. mansoni parasite. This dataset was originally published in Le Clec'h et al., 2019 (Striking differences in virulence, transmission and sporocyst growth dynamics between two schistosome populations. Parasites and Vectors. 2019 Oct 16;12(1):485. doi: 10.1186/s13071-019-3741-z).   This table is made of 9 columns: <ul> <li>id: the unique identifier of each sample.</li> <li>schistosoma_population: the population of schistosome used for the infection of the snail. Each snail was infected with a single parasite genotype. We have used SmLE (high shedder/highly virulent population) and SmBRE (low shedding/low virulent population).</li> <li>Shed.1: the number of cercariae produced by each parasite genotype at the first shedding week (4 weeks after exposure to parasite).</li> <li>Shed.2: the number of cercariae produced by each parasite genotype at the second shedding week (5 weeks after exposure to parasite).</li> <li>Shed.3: the number of cercariae produced by each parasite genotype at the third shedding week (6 weeks after exposure to parasite).</li> <li>Shed.4: the number of cercariae produced by each parasite genotype at the fourth shedding week (7 weeks after exposure to parasite).</li> <li>sum: the sum of the cercariae produced by each parasite genotype over the 4 weeks of shedding (Shed.1 + Shed.2 + Shed.3 + Shed.4).</li> <li>average: the average number of cercariae produced by each parasite genotype over the 4 weeks of shedding.</li> <li>sex: the sex of each parasite genotype determined by PCR 1.</li> </ul>   F1.csv   This table contains the number of cercariae produced by each individual Biomphalaria glabrata Bg26 snails infected with single genotypes of F1 progeny from the cross SmLE x SmBRE (see the manuscript for details).   This table is made of 11 columns: <ul> <li>id: the unique identifier of each sample.</li> <li>cross: F1A or F1B cross. Each snail was infected with a single parasite genotype from either F1A or F1B progeny.</li> <li>Shed.1: the number of cercariae produced by each parasite genotype at the first shedding week (4 weeks after exposure to parasite).</li> <li>Shed.2: the number of cercariae produced by each parasite genotype at the second shedding week (5 weeks after exposure to parasite).</li> <li>Shed.3: the number of cercariae produced by each parasite genotype at the third shedding week (6 weeks after exposure to parasite).</li> <li>Shed.4: the number of cercariae produced by each parasite genotype at the fourth shedding week (7 weeks after exposure to parasite).</li> <li>sum: the sum of the cercariae produced by each parasite genotype over the 4 weeks of shedding (Shed.1 + Shed.2 + Shed.3 + Shed.4).</li> <li>average: the average number of cercariae produced by each parasite genotype over the 4 weeks of shedding.</li> <li>PO: the total phenoloxidase activity in infected snail hemolymph, measured at 7.5 weeks post-exposure 2.</li> <li>Hb: the hemoglobin rate in infected snail hemolymph, measured at 7.5 weeks post-exposure 3.</li> <li>sex: the sex of each parasite genotype determined by PCR 1.</li> </ul>   F2.csv This table contains the number of cercariae produced by each individual Biomphalaria glabrata Bg26 snails infected with single genotypes of F2 progeny from the cross SmLE x SmBRE (see the manuscript for details).   This table is made of 10 columns: <ul> <li>id: the unique identifier of each sample.</li> <li>cross: F2A or F2B cross. Each snail was infected with a single parasite genotype from either F2A or F2B progeny.</li> <li>Shed.1: the number of cercariae produced by each parasite genotype at the first shedding week (4 weeks after exposure to parasite).</li> <li>Shed.2: the number of cercariae produced by each parasite genotype at the second shedding week (5 weeks after exposure to parasite).</li> <li>Shed.3: the number of cercariae produced by each parasite genotype at the third shedding week (6 weeks after exposure to parasite).</li> <li>Shed.4: the number of cercariae produced by each parasite genotype at the fourth shedding week (7 weeks after exposure to parasite).</li> <li>sum: the sum of the cercariae produced by each parasite genotype over the 4 weeks of shedding (Shed.1 + Shed.2 + Shed.3 + Shed.4)</li> <li>average: the average number of cercariae produced by each parasite genotype over the 4 weeks of shedding.</li> <li>PO: the total phenoloxidase activity in infected snail hemolymph, measured at 7.5 weeks post-exposure 2.</li> <li>Hb: the hemoglobin rate in infected snail hemolymph, measured at 7.5 weeks post-exposure 3.</li> </ul>   sex.csv   This table contains the in silico sexing of F0 parents, F1 parents and F2 progeny of S. mansoni parasites. This table is made of 4 columns: <ul> <li>id: the unique identifier of each sample</li> <li>read_depth: the read depth ratio between the Z-linked and pseudo-autosomal regions.</li> <li>ratio: computed ratio between the Z-linked and pseudo-autosomal regions.</li> <li>sex: the sex of each parasite genotype determined in silico: a ratio around 1 corresponds to a male carrying two Z chromosomes while a ratio around 0.5 corresponds to a female carrying only one Z chromosome.</li> </ul> Notes: 1. Le Clec’h W, Chevalier F et al. Real-time PCR for sexing Schistosoma mansoni cercariae. Mol Biochem Parasitol. Jan-Feb 2016; 205(1-2):35-8.doi: 10.1016/j.molbiopara.2016.03.010. Epub 2016 Mar 26. 2. Le Clec’h W et al. Characterization of hemolymph phenoloxidase activity in two Biomphalaria snail species and impact of Schistosoma mansoni infection. Parasit Vectors. 2016 Jan 22; 9:32.doi: 10.1186/s13071-016-1319-6. 3. Le Clec'h et al. Striking differences in virulence, transmission and sporocyst growth dynamics between two schistosome populations. Parasit Vectors. 2019 Oct 16; 12(1):485. doi: 10.1186/s13071-019-3741-z.

opencc-by-sa-4.0Sep 2024View details →

Genomic Typing, Antimicrobial Resistance Gene, Virulence Factor and Plasmid Replicon Dataset for the Important Pathogenic Bacteria Klebsiella pneumoniae

The infections caused by various bacterial pathogens both in clinical and community settings represent a significant threat to public healthcare worldwide. The growing resistance to antimicrobial drugs acquired by bacterial species causing healthcare-associated infections has already become a life-threatening danger noticed by the World Health Organization. Several groups or lineages of bacterial isolates usually called 'the clones of high risk' often drive the spread of resistance within particular species.  Thus, it is vitally important to reveal and track the spread of such clones and the mechanisms by which they acquire antibiotic resistance and enhance their survival skills. Currently, the analysis of whole genome sequences for bacterial isolates of interest is increasingly used for these purposes, including epidemiological surveillance and developing of spread prevention measures. However, the availability and uniformity of the data derived from the genomic sequences often represents a bottleneck for such investigations.  In this dataset, we present the results of a genomic epidemiology analysis of 61,857 genomes of a dangerous bacterial pathogen Klebsiella pneumoniae obtained from NCBI Genbank database. Important typing information including multilocus sequence typing (MLST)-based sequence types (STs), capsular (KL) and oligosaccharide (OL) types, CRISPR-Cas systems, and cgMLST profiles are presented, as well as the assignment of particular isolates to clonal groups (CG). The presence of antimicrobial resistance and virulence genes, as well as plasmid replicons, within the genomes is also reported.  These data will be useful for researchers in the field of K. pneumoniae genomic epidemiology, resistance analysis and prevention measure development.

opencc-by-4.0Dec 2021View details →

Cellular and Humoral Immune Responses after Immunisation with Low Virulent African Swine Fever Virus in the Large White Inbred Babraham Line and Outbred Domestic Pigs

Raw data for manuscript. Contains temperature, clinical scores, qPCR, blood cell numbers and immune responses over time for two groups of pigs immunised with low virulent African swine fever virus and challenged with highly virulent virus. Data for each panel or figure is displayed on a separate worksheet in the file. The readme worksheet contains a brief description of each figure. The majority of data is displayed in an XY table format, with the number of days post immunisation with low virulent virus indicated.

opencc-by-4.0Jul 2022View details →

A chromosome-level genome resource for studying virulence mechanisms and evolution of the coffee rust pathogen Hemileia vastatrix

Recurrent epidemics of coffee leaf rust, caused by the fungal pathogen Hemileia vastatrix, have constrained the sustainable production of Arabica coffee for over 150 years. The ability of H. vastatrix 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 H. vastatrix 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 H. vastatrix that, while useful, remain fragmented and do not represent chromosomal scaffolds. Here, we present a complete scaffolded pseudochromosome-level genome resource for H. vastatrix 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

opencc-by-4.0Sep 2024View details →

Data associated with "Microbiota-derived metabolites inhibit Salmonella virulent subpopulation development by acting on single-cell behaviors"

Data used for the publication Microbiota-derived metabolites inihibit Salmonella virulent subpopulation development by acting on single-cell behaviors.     all_hi_2307202.csv       Single-cell quantifications of Salmonella SPI-1 reporter cells grown in the presence of SCFAs. all_no_2307202.csv      Single-cell quantifications of Salmonella SPI-1 reporter cells grown in the absence of SCFAs. odmeasurements.csv     OD measurements of plate-reader assays of Salmonella SPI-1 reporter cells and controls grown in a range of SCFA conditions.   gfpmeasurements.csv    GFP measurements of plate-reader assays of Salmonella SPI-1 reporter cells and controls grown in a range of SCFA conditions.

opencc-by-4.0Nov 2022View details →

Development of a spectral library for the discovery of altered genomic events in Mycobacterium avium associated with virulence using mass spectrometry-based proteogenomic analysis

Mycobacterium avium is one of the prominent disease-causing bacteria in humans. It causes lymphadenitis, chronic and extrapulmonary, and disseminated infections in adults, children, and immunocompromised patients. M. avium has ~4,500 predicted protein-coding regions on an average, which can be helpful in discovering several variants at the proteome level. Many of them are potentially associated with virulence, thus identifying such proteins can be a helpful feature in the development of panel-based theranostics. In line with such a long-term goal, we carried out an in-depth proteomic analysis of M. avium with both data-dependent and data-independent acquisition methods. Further, a set of proteogenomic investigations were carried out using the protein database for Mycobacterium tuberculosis, and a genome six-frame translated database and a variant protein database of M. avium. A search of mass spectrometry data analysis against M. avium protein database resulted in the identification of 2,954 proteins. Further, proteogenomic analyses aided in the identification of 1,301 novel peptide sequences and correction of translation start sites for 15 proteins. At the end, we created a spectral library of M. avium proteins including novel genome search-specific peptides and variant peptides detected in this study. We validated the spectral library by a data-independent acquisition of the M. avium proteome. Thus, we present a M. avium spectral library of 29,033 peptide precursors supported by 0.4 million fragment ions for further use by the biomedical community.

opencc-by-4.0Apr 2020View details →

Virulence mismatches in index hosts shape the outcomes of cross-species transmission

Supplemental data and code for the paper Virulence mismatches in index hosts shape the outcomes of cross-species transmission. <ul> <li>Dataset 1 is an R Shiny app allowing the estimation of rabies disease progression parameters for all observed combinations of virus source (reservoir) and recipient species, including within-species inoculations.</li> <li>Dataset 2 contains the original data and the analysis code used in this study.</li> </ul> See the README files in each dataset folder for further information and usage instructions.

dryad40/100

Phage selection drives resistance-virulence trade-offs in Ralstonia solanacearum plant pathogenic bacterium irrespective of the growth temperature

While temperature has been shown to affect the survival and growth of bacteria and their phage parasites, it is unclear if trade-offs between phage resistance and other bacterial traits depend on the temperature. Here, we experimentally compared the evolution of phage resistance-virulence trade-offs and underlying molecular mechanisms in phytopathogenic Ralstonia solanacearum bacterium at 25 °C and 35 °C temperature environments. We found that experimental growth conditions selected for small colony variants (SCVs) with increased growth rate and mutations in the quorum-sensing (QS) signalling receptor gene, phcS. Interestingly, SCVs were also phage-resistant and reached higher frequencies in the presence of phages in both temperature environments. Evolving phage resistance was costly in terms of reduced carrying capacity, biofilm formation and reduced virulence in planta possibly due to loss of QS-mediated expression of key virulence genes. We also observed mucoid phage-resistant colonies that showed loss of virulence and reduced twitching motility likely due to parallel mutations in prepilin peptidase gene pilD. Moreover, phage-resistant SCVs from 35 °C-phage treatment had parallel mutations in genes encoding type II secretion system (T2SS) genes (gspE and gspF), indicating that defects in pseudopilus made bacterium resistant to the phage. Additional transcriptomic analysis revealed upregulation of CBASS and type Ⅰ restriction-modification phage defence systems in response to phage exposure, which coincided with reduced expression of motility and virulence-associated genes, including pilD and type II and III secretion systems. Together, these results suggest that phage resistance-virulence trade-offs are not affected by the growth temperature but can be mediated through both pre- and post-infection phage resistance mechanisms.

opencc-zeroNov 2023View details →

opencc-by-nc-sa-4.0Nov 2023View details →

The genomic and epidemiological virulence patterns of Salmonella enterica serovars in the United States

The serovars of Salmonella enterica display dramatic differences in pathogenesis and host preferences. We developed a process (patent pending) for grouping Salmonella isolates and serovars by their public health risk. We collated a curated set of 12,337 S. enterica isolate genomes from human, beef, and bovine sources in the US. After annotating a virulence gene catalog for each isolate, we used unsupervised random forest methods to estimate the proximity (similarity) between isolates based upon the genomic presentation of putative virulence traits  We then grouped isolates (virulence clusters) using hierarchical clustering (Ward's method), used non-parametric bootstrapping to assess cluster stability, and externally validated the clusters against epidemiological virulence measures from FoodNet, the National Outbreak Reporting System (NORS), and US federal sampling of beef products. We identified five stable virulence clusters of S. enterica serovars. Cluster 1 (higher virulence) serovars yielded an annual incidence rate of domestically acquired sporadic cases roughly one and a half times higher than the other four clusters combined (Clusters 2-5, lower virulence). Compared to other clusters, cluster 1 also had a higher proportion of infections leading to hospitalization and was implicated in more foodborne and beef-associated outbreaks, despite being isolated at a similar frequency from beef products as other clusters. We also identified subpopulations within 11 serovars. Remarkably, we found S. Infantis and S. Typhimurium subpopulations that significantly differed in genome length and clinical case presentation. Further, we found that the presence of the pESI plasmid accounted for the genome length differences between the S. Infantis subpopulations. Our results show that S. enterica strains associated with highest incidence of human infections share a common virulence repertoire. This work could be updated regularly and used in combination with foodborne surveillance information to prioritize serovars of public health concern.  Files contained in this repository will reproduce elements of figures 3,4,6, and 7 of the accompanying PLOS One manuscript.

dryad40/100

The effect of a temperature‐sensitive prophage on the evolution of virulence in an opportunistic bacterial pathogen

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 Serratia marcescens, 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 S. marcescens 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.

opencc-zeroSep 2022View details →

opencc-by-4.0Oct 2022View details →

Data for "Excess labile carbon promotes the expression of virulence factors in coral reef bacterioplankton"

This publication contains 27 coral reef bacterioplankton metagenome-assembled genomes (MAGs) from the following paper:  Cárdenas, A., Neave, M. J., Haroon, M. F., Pogoreutz, C., Rädecker, N., Wild, C., Gärdes, A., & Voolstra, C. R. (2018). Excess labile carbon promotes the expression of virulence factors in coral reef bacterioplankton. The ISME Journal, 12(1), 59–76. https://doi.org/10.1038/ismej.2017.142

Figure 2 in Biology, pathotype, and virulence of Globodera rostochiensis populations from Kenya

Figure 2: Figure showing the mean number of different developmental stages of Globodera rostochiensis, of 'HAR1' and 'Ecosse' populations in resistant cv. 'Laura' and susceptible cv. 'Désirée' in the glasshouse in the second experiment.

Figure 1 in Biology, pathotype, and virulence of Globodera rostochiensis populations from Kenya

Figure 1: Figure showing the mean number of different developmental stages of Globodera rostochiensis, 'HAR1' and 'Ecosse' populations in resistant cv. 'Laura' and susceptible cv. 'Désirée' in the glasshouse during the first experiment.

Figure 4 in Biology, pathotype, and virulence of Globodera rostochiensis populations from Kenya

Figure 4: Percentage hatch of Globodera rostochiensis 'HAR1' population in PRD for three successive generations of cysts without diapause. Vertical bars are mean percentage ± standard error (n = 4).

Figure 3 in Biology, pathotype, and virulence of Globodera rostochiensis populations from Kenya

Figure 3: Mean reproduction factor (±SE) of six populations of Globodera rostochiensis from Kenya on the susceptible cultivar 'Désirée' for three successive generations without diapause. Vertical bars show the standard error of the mean (n = 6). Means within a population with the same small letter are not significantly different (p> 0.05).