DOI: 10.6084/m9.figshare.13259828.v2
title: Data associated to the manuscript: "Ameline C, Bourgeois Y, Vögtli F, Savola E, Engelstädter Y, Andras J, Ebert D. 2020. A two-locus system with strong epistasis underlies rapid parasite-mediated evolution of host resistance. Mol. Biol. Evol. accepted".

description: Abstract Parasites are a major evolutionary force, driving adaptive responses in host populations. Although the link between phenotypic response to parasite-mediated natural selection and the underlying genetic architecture often remains obscure, this link is crucial for understanding the evolution of resistance and predicting associated allele frequency changes in the population. To close this gap, we monitored the response to selection during epidemics of a virulent bacterial pathogen, <i>Pasteuria ramosa</i>, in a natural host population of <i>Daphnia magna</i>. Across two epidemics, we observed a strong increase in the proportion of resistant phenotypes as the epidemics progressed. Field and laboratory experiments confirmed that this increase in resistance was caused by selection from the local parasite. Using a genome wide association study (GWAS), we built a genetic model in which two genomic regions with dominance and epistasis control resistance polymorphism in the host. We verified this model by selfing host genotypes with different resistance phenotypes and scoring their F1 for segregation of resistance and associated genetic markers. Such epistatic effects with strong fitness consequences in host-parasite coevolution are believed to be crucial in the Red Queen model for the evolution of genetic recombination. Usage Notes Data associated to the manuscript: "Ameline C, Bourgeois Y, Vögtli F, Savola E, Engelstädter Y, Andras J, Ebert D. 2020. A two-locus system with strong epistasis underlies rapid parasite-mediated evolution of host resistance. <em>Mol. Biol. Evol.</em> accepted". List of files<br> <br> ##################################################################<br> - Elocus_MBE.R: R script The R script uses the following files: <br> 1. Field monitoring of resistance and prevalence - chh20142015.txt: resistotype and prevalence data for 2014 and 2015<br> - chhcolorcode.txt: color code for resistotypes<br> - pasteuria_distri_2011: pasteuria genotypes dynamics in 2011<br> 2. Experimental and field infections - experimental_infections.csv: data from experimental infections in 2014<br> - field_infections.csv: data from field infections in 2015 <br>3. GWAS - orientation.txt: orientation info from reference genome<br> - plink.P1.assoc: association file from SS_S vs. RR_X<br> - plink.P2.assoc: association file from XX_S vs. RR_R<br> - plink.P3.assoc: association file from RR_R vs. RR_S<br> - plink.P4.assoc: association file from SS_S vs. RR_S<br> - plink.P5.assoc: association file from SS_S vs. RR_R <br>4. genetic crossings data for testing goodness of fit between observed and expected<br> segregation of resistotypes in F1 offspring groups - table0_geno.txt<br> - table0_pheno.txt<br> - table2_geno.txt<br> - table2_pheno.txt<br> - table4_geno.txt<br> - table4_pheno.txt<br> - table5_geno.txt<br> - table5_pheno.txt<br> - table6_geno.txt<br> - table6_pheno.txt<br> - table8_geno.txt<br> - table10_pheno.txt<br> - table11_pheno.txt <br> - DMPR1linkage.txt: data for test linkage of DMPR1 with C locus<br> - DMPR2linkage.txt: data for test linkage of DMPR2 with C locus<br> - DMPR3linkage.txt: data for test linkage of DMPR3 with E locus<br> - DMPR4linkage.txt: data for test linkage of DMPR1 with E locus ##################################################################