Additional file 1: of Variation and correlations between sexual, asexual and natural enemy resistance life-history traits in a natural plant pathogen population
Creators: name: Numminen, Elina
name: Vaumourin, Elise
name: Parratt, Steven
name: Poulin, Lucie
name: Anna-Liisa Laine
Publisher: name: figshare
Year: 2019
Subjects: subject: Medicine
subject: Ecology
subject: FOS: Biological sciences
subject: FOS: Biological sciences
subject: 110309 Infectious Diseases
subject: FOS: Health sciences
subject: FOS: Health sciences
subject: Computational Biology

description: Figure S1. Summary of the experimental design. Table S1. The number of of inoculations per strain in each experiment block. Table S2. The total numbers of inoculations that germinated for each strain. Table S3. The total numbers of inoculations that resulted in immature and mature chasmothecia. Table S4. The number of Ampelomyces hyperparasite inoculations that reached state A1 for each powdery mildew strain. Table S5. The number of Ampelomyces hyperparasite inoculations that reached hyperparasite state A2 for each powdery mildew strain. Table S6. Typer4 Parameters for genotyping calling. Figure S2. Panel (A) displays the locations in which the studied strains were found in 2015. Majority (395) of all the strains found that year were only found in one location. Panel (B) shows the frequency distribution for the number of occupied locations for all the strains, for the SNP panel of 19 SNPs together with the locus with contig ID c6190. The study strains are shown in colors, and the amounts of colonized locations for each strain are shown in parenthesis. The shape_les used for generating the maps in panel A were downloaded from Stanford digital repository ( https://purl.stanford.edu/np067sb6776 ). Figure S3. Powdery mildew growth was scored using Bevan’s scale (adapted from [7]), ranging from 0 to 4 (0: no mycelium, 1: mycelium only, 2: mycelium and sparse sporulation visible only under a dissecting microscope, 3:abundant sporulation and lesion size 0.5 cm2). Figure S4. Ampelomyces infection was scored with a modi_ed version of the scale reported in [16]: A0: no pycnidia observed, A1: 1–20 pycnidia in each Ampelomyces cluster appearing and A2: 20–50 pycnidia in each powdery mildew lesion or between 30 and 50% of powdery mildew covered. This scale can re_ect either a set number of Ampelomyces pycnidia or an estimate of pycnidia coverage of the powdery mildew lesion. Hence, the scale controls for the di_erent amounts of powdery mildew tissue available for the hyperparasite to infect, i.e. small powdery mildew lesions can still support hyperparasite infection state A2 even if there is not enough tissue to produce abundant pycnidia. Table S7. The means and standard deviations of the measured life-history traits. Summary statistics for the timings of life-history events are computed only for inoculations for which the event actually occurred. The largest average value in each row is indicated in red, and the smallest in blue. Table S8. The results from pairwise model comparisons, for the survival models where the model with only strain id and the same model with both the experiment id and strain id as predictors are contrasted using anova. The presented p-value corresponds to the evidence in favor of the more rich model (Model 2). Table S9. The results from pairwise model comparisons, for the survival models where the model with only experiment id and the same model with both the experiment id and strain id as predictors are contrasted using anova. The presented p-value corresponds to the evidence in favor of the more rich model (Model 2). Table S10. The estimated relative rates and their 95% con_dence intervals for the di_erent studied infection event times, together with the associated test statistic for rejecting the null hypothesis of the corresponding factor having no e_ect on the rate of the event. Signi_cant deviations are shown in bold. Table S11. The results from pairwise model comparisons, for the ordinal regression models where the model with only experiment id and the same model with both the experiment id and strain id as predictors are contrasted using anova. The presented p-value corresponds to the evidence in favor of the more rich model (Model 2). Table S12. The results from pairwise model comparisons, for the ordinal regression models where the model with only strain id and the same model with both the experiment id and strain id as predictors are contrasted using anova. The presented p-value corresponds to the evidence in favor of the more rich model (Model 2). Table S13. Estimated e_ects for the ordinal regression model for the Bevan scale at day 15. Signi_cant deviations are shown in bold. Table S14. Estimated e_ects for the ordinal regression model for the (immature) chasmothecia category by the end of the follow-up. Table S15. The estimated relative rates (exponentials of the estimated coe_cients) for using the columns as predictor when predicting the event times indicated by the rows. The statistical signi_cancy of the estimated e_ect is shown in parenthesis and the signi_cant e_ects are shown in bold. With NA’s we have omitted the pairs of events occurring in wrong order, as they lead to non-intuitive modelling, as well as. Table S16. The estimated e_ects of event timings (columns) as predictor when predicting the abundance measureds indicated by the rows. The statistical signi_cancy of the estimated e_ect is shown in parenthesis and the signi_cant e_ects are shown in bold. Table S17. The estimated relative rates (exponentials of the estimated coe_cients) for using event times in the columns as predictor for the hyperparasite infection event times, indicated by the rows. The statistical signi_cancy of the estimated e_ect is shown in parenthesis and the signi_cant e_ects are shown in bold. Table S18. The results from pairwise model comparisons, for the survival models presented in where a survival model without any predictors and a model with the strain as a predictor are contrasted using anova. The presented p-value corresponds to the evidence in favor of the more rich model (Model 2). Table S19. The results from pairwise model comparisons, for survival models where a survival model with strain id as a predictor and a model with the strain and pathogen infection status at day 8 as a predictor are contrasted using anova. The presented p-value corresponds to the evidence in favor of the more rich model (Model 2). Table S20. The results from pairwise model comparisons, for the survival models where a survival model with pathogen infection status at day 8 as a predictor and a model with the strain id and pathogen infection status at day 8 as a predictor are contrasted using anova. The presented p-value corresponds to the evidence in favor of the more rich model (Model2). Table S21. The estimated relative rates and their 95% con_dence intervals for the di_erent studied hyperparasite infection event times, together with the associated test statistic for rejecting the null hypothesis of the corresponding factor having no e_ect on the rate of the event. Signi_cant deviations are shown in bold. Table S22. The estimated relative rates and their 95% con_dence intervals for the di_erent studied hyperparasite infection event times, where in the model the pathogen infection stage at day 8 was accounted for, together with the associated test statistic for rejecting the null hypothesis of the corresponding factor having no e_ect on the rate of the event. Signi_cant deviations are shown in bold. Figure S5. Panel A shows the frequency distribution for the number of occupied locations for all the observed strains in 2015. The majority of observed strains (395) in that year were only found in a single location, but 3 strains were found in &gt; 25 discrete locations. Strains used to study life-history variation are shown in color. In panel B the prevalence of strains across the metapopulation is correlated with the mean _tness traits, and the corresponding p-values for the _tted rank correlations are shown in upright. (PDF 1859 kb)