Lake location, zooplankton species abundance and body size data

This file contains the raw data used in all analyses. Within the file is the zooplankton species composition from 2011 (relative abundance) and historical samples (relative abundance and presence/absence). In addition, body length data (micrometers) for a subset of the lakes is present. Finally, geographic coordinates for each lake (latitude/longitude) are in the data file

Empirical evidence that metabolic theory describes the temperature dependency of within-host parasite dynamics

<div><p>The complexity of host–parasite interactions makes it difficult to predict how host–parasite systems will respond to climate change. In particular, host and parasite traits such as survival and virulence may have distinct temperature dependencies that must be integrated into models of disease dynamics. Using experimental data from <i>Daphnia magna</i> and a microsporidian parasite, we fitted a mechanistic model of the within-host parasite population dynamics. Model parameters comprising host aging and mortality, as well as parasite growth, virulence, and equilibrium abundance, were specified by relationships arising from the metabolic theory of ecology. The model effectively predicts host survival, parasite growth, and the cost of infection across temperature while using less than half the parameters compared to modeling temperatures discretely. Our results serve as a proof of concept that linking simple metabolic models with a mechanistic host–parasite framework can be used to predict temperature responses of parasite population dynamics at the within-host level.</p></div

Observed (filled circles, ± 95% CI shown in b) and predicted mean lifespans of hosts from DT (a: unfilled squares and triangles) and MTE (b: solid and dotted lines) models, as well as the MTE-predicted percentage cost of infection across the temperature range (c).

<p>The DT model can only predict mean lifespan at the nine temperatures where we have observed data, whereas the MTE model is able to make predictions across any temperature range of interest. The data used to make this figure can be found in <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.2004608#pbio.2004608.s013" target="_blank">S1 Data</a>. DT, discrete temperature; MTE, metabolic theory of ecology.</p

MLEs and SE for the hyperparameters associated with metabolic models for each of the host–parasite parameters (S1 Table) from 25 clones of the data.

<p>The MCMC chains converged for all parameters (), but some parameters were not estimable and are highlighted in grey.</p

Maximum likelihood estimates ± 95% confidence intervals for the DT model (points and vertical bars) and fitted MTE functions ± 95% confidence intervals (lines and shaded region) for host–parasite model parameters: a) natural host mortality <i>μ</i>, b) natural mortality shape parameter for unexposed individuals <i>β</i>_U, c) natural mortality shape parameter for exposed individuals <i>β</i>_E, d) parasite growth rate <i>r</i>, e) parasite equilibrium abundance <i>θ</i>, and f) parasite virulence <i>α</i>.

<p><i>β</i>_<i>U</i> (unexposed data) and <i>β</i>_<i>E</i> (exposed data) were estimated separately for DT estimates, but shared the same MTE function (Sharpe–Schoolfield with upper threshold). The 95% confidence interval on MTE model predictions was calculated as the 95% quantiles of 1,000 Monte Carlo samples of the host–parasite model parameters; in each Monte Carlo sample, the associated hyperparameters were chosen from a normal distribution with mean and SE of the MLE. Parameters that were not estimable are not shown (see <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.2004608#pbio.2004608.s015" target="_blank">S1 Text</a> for details). DT, discrete temperature; MTE, metabolic theory of ecology.</p

The number of parasites per exposed individual at TOD.

<p>Circles show nonzero parasite loads at TOD, while crosses represent exposed individuals who had zero parasites at TOD. Model fits are shown by the dashed (DT) and dotted (MTE) lines. Parasites were never observed at 6.0 °C, 9.5 °C, or 33.3 °C. The DT model does not make predictions for exposed individuals at 6.0 °C, 9.5 °C, 29.7 °C, or 33.3 °C due to convergence and estimability issues for some of the parasite-related parameters. The data used to make this figure can be found in <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.2004608#pbio.2004608.s013" target="_blank">S1 Data</a>. DT, discrete temperature; MTE, metabolic theory of ecology; TOD, time of death.</p

Summary of experimental data.

<p>Infection % is the percent of exposed individuals that were infected upon inspection at death. Infection intensity is the number of spore clusters in an individual at death and was calculated using only individuals who had a nonzero parasite load. Mean survival time was calculated for the entire treatment sample, including exposed individuals with parasite load zero.</p

Solid lines show the proportion of unexposed (<i>n</i> = 195; blue) and exposed (<i>n</i> = 355; red) individuals surviving over the course of the 285-d experiment.

<p>Model fits are shown by the dashed (DT) and dotted (MTE) lines. The DT model does not make predictions for exposed individuals at 6.0 °C, 9.5 °C, 29.7 °C, or 33.3 °C due to convergence and estimability issues for some of the parasite-related parameters. The data used to make this figure can be found in <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.2004608#pbio.2004608.s013" target="_blank">S1 Data</a>. DT, discrete temperature; MTE, metabolic theory of ecology.</p

GSEA for loss of chromosomal bands.

<p>Footnote. The genes column shows the number of genes used to score the band. The nominal, FDR and FWER p-values were all <0.001. ES, enrichment score; NES normalized enrichment score.</p

ROC analysis of the <i>BRCA2</i> signature in the validation set.

<p>Each tumor was given a score that was a weighted sum of the mean centered gene expression levels for each gene in the signature. The validation set contained 19 <i>BRCA2</i> and 12 <i>BRCAX</i> tumors. The AUC was 0.76.</p