No abstract

SignificancePathogens are omnipresent and by definition detrimental to their hosts. Pathogens thus exert high selection on their hosts, which, if adapting, can exert similar levels of selection on the pathogen, resulting in ongoing cycles of reciprocal adaptation between the antagonists. Such coevolutionary interactions have a central influence on the evolution of organisms. Surprisingly, we still know little about the exact selection dynamics and the genome regions involved. Our study uses a controlled experimental approach with an animal host to dissect coevolutionary selection. We find that distinct selective processes underlie rapid coadaptation in the two antagonists, including antagonistic frequency-dependent selection on toxin gene copy number in the pathogen, while the host response is likely influenced by changes in multiple genome regions.

Understanding the genetic basis of complex traits remains a major challenge in biology. Polygenicity, phenotypic plasticity and epistasis contribute to phenotypic variance in ways that are rarely clear. This uncertainty is problematic for estimating heritability, for predicting individual phenotypes from genomic data, and for parameterizing models of phenotypic evolution. Here we report a recombinant inbred line (RIL) quantitative trait locus (QTL) mapping panel for the hermaphroditic nematode Caenorhabditis elegans, the C. elegans multiparental experimental evolution (CeMEE) panel. The CeMEE panel, comprising 507 RILs, was created by hybridization of 16 wild isolates, experimental evolution at moderate population sizes and predominant outcrossing for 140-190 generations, and inbreeding by selfing for 13-16 generations. The panel contains 22% of single nucleotide polymorphisms known to segregate in natural populations, and complements existing mapping resources for C. elegans by providing high nucleotide diversity across >95% of the genome. We apply it to study the genetic basis of two fitness components, fertility and hermaphrodite body size at time of reproduction, with high broad sense heritability in the CeMEE. While simulations show we should detect common alleles with additive effects as small as 5%, at gene-level resolution, the genetic architectures of these traits does not feature such alleles. We instead find that a significant fraction of trait variance, particularly for fertility, can be explained by sign epistasis with weak main effects. In congruence, phenotype prediction, while generally poor (r 2 < 10%), requires modeling epistasis for optimal accuracy, with most variance attributed to the highly recombinant, rapidly evolving chromosome arms.

Using a new experimentally evolved multiparent mapping resource for C. elegans, Noble et al. have outlined the genetic architecture of worm fertility..