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326 results for “genetic architecture”
Phenotypic data related to genetic architecture of transmission stage production and virulence in schistosome parasites
<p>These data were generated related to the study of the <strong>Genetic architecture of transmission stage production and virulence in schistosome parasites</strong>.</p> <p><strong>Abstract:</strong> 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 <em>Schistosoma mansoni</em>, 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 <em>Biomphalaria glabrata</em> 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.</p> <p> </p> <p>This dataset is made of 4 tables:</p> <ul> <li>F0_parental_populations.csv</li> <li>F1.csv</li> <li>F2.csv</li> <li>sex.tsv</li> </ul> <p> </p> <p><strong>F0_parental_populations.csv</strong></p> <p> </p> <p>This table contains the number of cercariae produced by each individual <em>Biomphalaria glabrata</em> Bg26 snails infected with single genotypes of <em>Schistosoma mansoni</em> parasite. We have compared the transmission stage production between two different populations of <em>S. mansoni</em> 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).</p> <p> </p> <p>This table is made of 9 columns:</p> <ul> <li><strong>id</strong>: the unique identifier of each sample.</li> <li><strong>schistosoma_population</strong>: 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><strong>Shed.1</strong>: the number of cercariae produced by each parasite genotype at the first shedding week (4 weeks after exposure to parasite).</li> <li><strong>Shed.2</strong>: the number of cercariae produced by each parasite genotype at the second shedding week (5 weeks after exposure to parasite).</li> <li><strong>Shed.3</strong>: the number of cercariae produced by each parasite genotype at the third shedding week (6 weeks after exposure to parasite).</li> <li><strong>Shed.4</strong>: the number of cercariae produced by each parasite genotype at the fourth shedding week (7 weeks after exposure to parasite).</li> <li><strong>sum</strong>: 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><strong>average</strong>: the average number of cercariae produced by each parasite genotype over the 4 weeks of shedding.</li> <li><strong>sex</strong>: the sex of each parasite genotype determined by PCR <sup>1</sup>.</li> </ul> <p> </p> <p><strong>F1.csv</strong></p> <p> </p> <p>This table contains the number of cercariae produced by each individual <em>Biomphalaria glabrata</em> Bg26 snails infected with single genotypes of F1 progeny from the cross SmLE x SmBRE (see the manuscript for details).</p> <p> </p> <p>This table is made of 11 columns:</p> <ul> <li><strong>id</strong>: the unique identifier of each sample.</li> <li><strong>cross</strong>: F1A or F1B cross. Each snail was infected with a single parasite genotype from either F1A or F1B progeny.</li> <li><strong>Shed.1</strong>: the number of cercariae produced by each parasite genotype at the first shedding week (4 weeks after exposure to parasite).</li> <li><strong>Shed.2</strong>: the number of cercariae produced by each parasite genotype at the second shedding week (5 weeks after exposure to parasite).</li> <li><strong>Shed.3</strong>: the number of cercariae produced by each parasite genotype at the third shedding week (6 weeks after exposure to parasite).</li> <li><strong>Shed.4</strong>: the number of cercariae produced by each parasite genotype at the fourth shedding week (7 weeks after exposure to parasite).</li> <li><strong>sum</strong>: 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><strong>average</strong>: the average number of cercariae produced by each parasite genotype over the 4 weeks of shedding.</li> <li><strong>PO</strong>: the total phenoloxidase activity in infected snail hemolymph, measured at 7.5 weeks post-exposure <sup>2</sup>.</li> <li><strong>Hb</strong>: the hemoglobin rate in infected snail hemolymph, measured at 7.5 weeks post-exposure <sup>3</sup>.</li> <li><strong>sex</strong>: the sex of each parasite genotype determined by PCR <sup>1</sup>.</li> </ul> <p> </p> <p><strong>F2.csv</strong></p> <p>This table contains the number of cercariae produced by each individual <em>Biomphalaria glabrata</em> Bg26 snails infected with single genotypes of F2 progeny from the cross SmLE x SmBRE (see the manuscript for details).</p> <p> </p> <p>This table is made of 10 columns:</p> <ul> <li><strong>id</strong>: the unique identifier of each sample.</li> <li><strong>cross</strong>: F2A or F2B cross. Each snail was infected with a single parasite genotype from either F2A or F2B progeny.</li> <li><strong>Shed.1</strong>: the number of cercariae produced by each parasite genotype at the first shedding week (4 weeks after exposure to parasite).</li> <li><strong>Shed.2</strong>: the number of cercariae produced by each parasite genotype at the second shedding week (5 weeks after exposure to parasite).</li> <li><strong>Shed.3</strong>: the number of cercariae produced by each parasite genotype at the third shedding week (6 weeks after exposure to parasite).</li> <li><strong>Shed.4</strong>: the number of cercariae produced by each parasite genotype at the fourth shedding week (7 weeks after exposure to parasite).</li> <li><strong>sum</strong>: 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><strong>average</strong>: the average number of cercariae produced by each parasite genotype over the 4 weeks of shedding.</li> <li><strong>PO</strong>: the total phenoloxidase activity in infected snail hemolymph, measured at 7.5 weeks post-exposure <sup>2</sup>.</li> <li><strong>Hb</strong>: the hemoglobin rate in infected snail hemolymph, measured at 7.5 weeks post-exposure <sup>3</sup>.</li> </ul> <p> </p> <p><strong>sex.csv</strong></p> <p> </p> <p>This table contains the <em>in silico</em> sexing of F0 parents, F1 parents and F2 progeny of <em>S. mansoni</em> parasites.</p> <p>This table is made of 4 columns:</p> <ul> <li><strong>id</strong>: the unique identifier of each sample</li> <li><strong>read_depth</strong>: the read depth ratio between the Z-linked and pseudo-autosomal regions.</li> <li><strong>ratio</strong>: computed ratio between the Z-linked and pseudo-autosomal regions.</li> <li><strong>sex</strong>: the sex of each parasite genotype determined <em>in silico</em>: 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> <p><strong>Notes:</strong></p> <p><sup>1</sup>. 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.</p> <p><sup>2</sup>. 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.</p> <p><sup>3</sup>. 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.</p>
Genetic Architecture Reconciles Linkage and Association Studies of Complex Traits
<p>This (zipped) folder contains 3 sub-folders:</p> <p>#**********************************************************************************************************<br>The "bin" folder contains fuctions and gentic maps needed for analyes<br>bin \<br> predLink.R - function to predict linkage <br> sibREML_v0.1.1.R - function to run SibREML<br> sim-sib-array.R - script to simulate sib-pairs from parental haplotypes<br> Summarised_genetic_map_bcf.txt - genetic map per 0.5-cM long segments, based on map from bcftools <br> (BCFtools: https://samtools.github.io/bcftools/bcftools.html)<br> Summarised_genetic_map_OMNI.txt - genetic map per 0.5-cM long segments, based on OMNI map <br> (https://github.com/joepickrell/1000-genomes-genetic-maps/tree/master/interpolated_OMNI)<br>#**********************************************************************************************************</p> <p> </p> <p>#**********************************************************************************************************<br>The "SIM" folder contains the simulation pipeline (scripts 01-15) as well as IBD sharing and simulated phenotypes for Simulated sib-pairs.<br>SIM \<br> 01_sim-sib-array.sh *pre-run*<br> 02_bed_recode_bcf_map.sh *pre-run*<br> 03_make_merlin.R *pre-run*<br> 04_error_merlin.sh *pre-run*<br> 05_merlin_IBD.sh *pre-run*<br> 06_sample_causal_snps.R *pre-run*<br> 07_simulate_pheno.sh *pre-run*<br> 08_bhat_gwas.R *can be run using provided data* <br> 09_Linkage_VH.R *can be run using provided data* <br> 10_predLink.R *can be run using provided data*<br> 11_phi_hat.R *can be run using provided data*<br> 12_IBD_Mb.R *can be run using provided data*<br> 13_IBD_cM_recombrate_stratified.R *can be run using provided data*<br> 14_SibREML.R *can be run using provided data*<br> 15_SibREML_stratified_Q4.R *can be run using provided data*<br> causal_snps \ *provided causal SNPs*<br> IBD_results \ *provided IBD-probabilities for 1000 simulated sib-pairs*<br> Linkage_VH_results \ <br> pheno \ *provided simulated phenotypes (h2=1) for 8 genetic architectures*<br> Phi_hat_results.txt<br> predicted \<br> README<br> SibREML_results.txt<br> SibREML_stratified_Q4.txt</p> <p>The data can be used to run Linkage analysis, predict linkage, estimate phi_hat, <br>as well as estimate non-stratified and recombination rate stratified sib-heritability (h2_FS and c).<br>The README is provided within the folder. <br>#**********************************************************************************************************</p> <p> </p> <p>#**********************************************************************************************************<br>The "HT_BMI" folder contains data and scripts to predict linkage and estimate phi_hat for height and BMI.<br>HT_BMI \<br> 01_predLink_HT_BMI.R<br> 02_phi_hat_HT_BMI.R<br> gws_sumstats \ *provided summary GWAS summary statistics to predict linkage for height and BMI*<br> Linkage_results \ *provided linkage meta-analysis results for height and BMI from this study*<br> Phi_hat_results_HT_BMI.txt<br> PREDLINK_bmi.txt<br> PREDLINK_height.txt<br> README<br>The README is provided within the folder.<br>#**********************************************************************************************************</p> <p><strong> </strong></p>
Genetic architecture of immune cell DNA methylation in the rhesus macaque
<p><strong>Complete model outputs from rhesus macaque (<em>Macaca mulatta</em>) whole blood meQTL and eQTL analyses in article, "Genetic architecture of immune cell DNA methylation in the rhesus macaque". </strong></p> <p><strong><em>cis</em> meQTL model output (SNP-CpG associations):</strong> </p> <ol> <li>IMAGE_573_meqtl_model_res_wPVE.txt: <ul> <li>Model results from IMAGE meQTL mapping including all genome, chromatin state annotations, and PVE estimates</li> </ul> </li> <li>pqlseq_allimagesnps_res_converged_wpve.txt: <ul> <li>Model results from PQLseq meQTL mapping including PVE estimates </li> </ul> </li> </ol> <p><strong><em>cis</em> eQTL model output (SNP-gene associations): </strong></p> <ol> <li>eqtl_res_sva5_gemma_172samples_qvalue.txt: <ul> <li>Model results from GEMMA eQTL mapping </li> </ul> </li> </ol> <p> </p>
On the genetic architecture of rapidly adapting and convergent life history traits in guppies
<p>The genetic basis of traits shapes and constrains how adaptation proceeds in nature; rapid adaptation can be facilitated by polygenic traits, which subsequently provide multiple, redundant, genetic routes to adaptive phenotypes, reducing re-use of the same genes (genetic convergence). Guppy life history traits evolve rapidly and convergently among natural high- (HP) and low-predation (LP) environments in northern Trinidad. This system has been studied extensively at the phenotypic level, but little is known about the underlying genetic architecture. Here, we use an F2 QTL design to examine the genetic basis of seven (five female, two male) guppy life history phenotypes to assess whether the genetic architecture of these traits reflects theoretical predictions. We use RAD-sequencing data (16,539 SNPs) from 370 male and 267 female F2 individuals. We perform linkage mapping, estimates of genome-wide and per-chromosome heritability (multi-locus associations), and QTL ma pping (single-locus associations). Our results are consistent with architectures of many-loci of small effect for male age and size at maturity and female interbrood period. Male trait associations are clustered on specific chromosomes, but female interbrood period exhibits a weak genome-wide signal suggesting a potentially highly polygenic component. Offspring weight and female size at maturity are also associated with a single significant QTL each. These results suggest rapid phenotypic evolution of guppies may be facilitated by polygenic trait architectures, but these could fuel redundancy and limit gene re-use across populations, in agreement with an absence of strong signatures of genetic convergence from recent population genomic analyses of wild HP-LP guppies.</p>
Additional files for manuscript titled 'The double round-robin population unravels the genetic architecture of grain size in barley'
<p>Additional file 1: Parental allele for barley orthologs of genes controlling grain size in rice</p> <p>Additional file 2: Cross-validation of quantitative trait loci (QTLs) detected for grain size characters in rice</p> <p>Additional file 3: Adjusted entry means of recombinant inbred lines of 45 HvDRR sub-populations</p>
Genetic architecture of adaptive radiation across two trophic levels
<p>Evolution of trophic diversity is a hallmark of adaptive radiation. Yet, transitions between carnivory and herbivory are rare in young adaptive radiations. Haplochromine cichlid fish of the African Great Lakes are exceptional in this regard. Lake Victoria was colonized by an insectivorous generalist and in less than 20,000 years, several clades of specialized herbivores evolved. Carnivorous versus herbivorous lifestyles in cichlids require many different adaptations in functional morphology, physiology, and behaviour. Ecological transitions in either direction thus require many traits to change in a concerted fashion, which could be facilitated if genomic regions underlying these traits were physically linked or pleiotropic. However, linkage/pleiotropy could also constrain evolvability. To investigate components of the genetic architecture of a suite of traits that distinguish invertivores from algae scrapers, we performed Quantitative Trait Locus (QTL) mapping using a second-generation hybrid cross. While we found indications of linkage/pleiotropy within trait complexes, QTLs for distinct traits were distributed across several unlinked genomic regions. Thus, a mixture of independently segregating variation and some pleiotropy may underpin the rapid trophic transitions. We argue that the emergence and maintenance of associations between the different genomic regions underpinning co-adapted traits that evolved and persist against some gene flow required reproductive isolation.</p>
Genetic architecture of disease resistance and tolerance in Douglas-fir trees
<p><span>Understanding the genetic architecture of tolerance and resistance to pathogens is important to monitor and maintain resilient tree populations. Here we investigate the genetic basis of tolerance and resistance to needle cast disease in Douglas-fir (<em>Pseudotsuga menziesii</em>) caused by two fungal pathogens: Swiss needle cast (SNC) caused by <em>Nothophaeocryptopus gaeumannii</em>, and Rhabdocline needle cast (RNC) caused by <em>Rhabdocline pseudotsugae</em>). We performed a case-control genome-wide association analysis (GWA) and found these traits to be polygenic and under selection.</span> <span>We showed that stomatal regulation as well as ethylene and jasmonic acid pathways are important for resisting SNC infection and secondary metabolite pathways play a role in tolerating SNC once the plant is infected. We identified a key upstream transcription factor of plant defence, ERF1, as the main candidate for RNC resistance. Our findings contribute to the understanding of the highly polygenic architectures underlying disease resistance and tolerance in Douglas-fir and have important implications for forestry and conservation as the climate changes.</span></p>
Data from: Genome-wide association mapping within a local Arabidopsis thaliana population more fully reveals the genetic architecture for defensive metabolite diversity
<p>A paradoxical finding from genome-wide association studies (GWAS) in plants is that variation in metabolite profiles typically maps to a small number of loci, despite the complexity of underlying biosynthetic pathways. This discrepancy may partially arise from limitations presented by geographically diverse mapping panels. Properties of metabolic pathways that impede GWAS by diluting the additive effect of a causal variant, such as allelic and genic heterogeneity and epistasis, would be expected to increase in severity with the geographic range of the mapping panel. We hypothesized that a population from a single locality would reveal an expanded set of associated loci. We tested this in a French <em>Arabidopsis thaliana</em> population (< 1 km transect) by profiling and conducting GWAS for glucosinolates, a suite of defensive metabolites that have been studied in depth through functional and genetic mapping approaches. For two distinct classes of glucosinolates, we discovered more associations at biosynthetic loci than previous GWAS with continental-scale mapping panels. Candidate genes underlying novel associations were supported by concordance between their observed effects in the TOU-A population and previous functional genetic and biochemical characterization. Local populations complement geographically diverse mapping panels to reveal a more complete genetic architecture for metabolic traits.</p>
Data from the manuscript 'Accurate detection of shared genetic architecture from GWAS summary statistics in the small-sample context'
<p>Data sets from the manuscript 'Accurate detection of shared genetic architecture from GWAS summary statistics in the small-sample context'. These include the test statistics from analyses of real and simulated data, and the data used to generate the figures relating to the goodness-of-fit of the generalised extreme value distribution to the GPS test statistics under the null. Please see the enclosed README for more details.</p>
Genetic architecture of dispersal behaviour in the post-harvest pest and model organism Tribolium castaneum
<p>Dispersal behaviour is an important aspect of the life-history of animals. However, the genetic architecture of dispersal related traits is often obscure or unknown, even in well studied species.<em> Tribolium castaneum</em> is a globally significant post-harvest pest and established model organism, yet studies of its dispersal have shown ambiguous results and the genetic basis of this behaviour remains unresolved. We combine experimental evolution and agent-based modelling to investigate the number of loci underlying dispersal in <em>T.castaneum</em>, and whether the trait is sex-linked. Our findings demonstrate rapid evolution of dispersal behaviour under selection. We find no evidence of sex-biases in the dispersal behaviour of the offspring of crosses, supporting an autosomal genetic basis of the trait. Moreover, simulated data approximates experimental data under simulated scenarios where the dispersal trait is controlled by one or few loci, but not many loci. Levels of dispersal in experimentally inbred lines, compared with simulations, indicate that a single locus model is not well supported. Taken together, these lines of evidence support an oligogenic architecture underlying dispersal in <em>Tribolium castaneum</em>. These results have implications for applied pest management and for our understanding of the evolution of dispersal in the coleoptera, the world's most species-rich order.</p>
The relative strength of selection on modifiers of genetic architecture under migration load
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Data from: Genome-wide association mapping within a local Arabidopsis thaliana population more fully reveals the genetic architecture for defensive metabolite diversity
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Data from: The genetic architecture of quantitative variation in the self-incompatibility response within Phlox drummondii (Polemoniaceae)
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Genetic architecture of adaptive radiation across two trophic levels
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Data from: Repeated evolution of photoperiodic plasticity by different genetic architectures during recurrent colonizations in a butterfly
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Genetic architecture of dispersal behaviour in the post-harvest pest and model organism Tribolium castaneum
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Genetic architecture of disease resistance and tolerance in Douglas-fir trees
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Genetic architecture underlying response to the fungal pathogen Dothistroma septosporum in lodgepole pine, jack pine, and their hybrids
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Data from: The genetic architecture of dewlap pattern in Hispaniola Anoles (Anolis distichus)
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On the genetic architecture of rapidly adapting and convergent life history traits in guppies
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