JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. abstract: Recent studies show that intraspecific genetic variation in asexual species may have large effects on community and ecosystem functions, increasing their stability, productivity, and species richness. However, major questions regarding its population-level impact remain empirically unanswered: (a) How does intraspecific genetic diversity affect the ecological characteristics of sexual species, in which recombination can alter the outcome of causal mechanisms such as selection and niche diversification? (b) Does genetic diversity increase population dynamic stability? (c) Is the impact of genetic diversity dependent on the selective environment? To answer these questions, I founded replicate flour beetle (Tribolium castaneum) populations with different degrees of ecologically relevant, heritable trait variation and monitored their dynamics for approximately eight generations. I show that population stability and persistence increased with greater genetic variation but that the stabilizing effect was independent of the selective habitat (different proportions of ancestral and novel resources). Alleles from a single founding strain underwent a selective sweep in the homogeneous ancestral habitat but not in a novel heterogeneous habitat. These results expand current understanding of the ecological impacts of genetic diversity by showing that genetically more diverse sexual populations persist longer and are more stable but that the selective environment determines the mechanistic basis of increased stability.

Biased codon usage in protein-coding genes is pervasive, whereby amino acids are largely encoded by a specific subset of possible codons. Within individual genes, codon bias is stronger at evolutionarily conserved residues, favoring codons recognized by abundant tRNAs. Although this observation suggests an overall pattern of selection for translation speed and/or accuracy, other work indicates that transcript structure or binding motifs drive codon usage. However, our understanding of codon bias evolution is constrained by limited experimental data on the fitness effects of altering codons in functional genes. To bridge this gap, we generated synonymous variants of a key enzyme-coding gene in Methylobacterium extorquens. We found that mutant gene expression, enzyme production, enzyme activity, and fitness were all significantly lower than wild-type. Surprisingly, encoding the gene using only rare codons decreased fitness by 40%, whereas an allele coded entirely by frequent codons decreased fitness by more than 90%. Increasing gene expression restored mutant fitness to varying degrees, demonstrating that the fitness disadvantage of synonymous mutants arose from a lack of beneficial protein rather than costs of protein production. Protein production was negatively correlated with the frequency of motifs with high affinity for the anti-Shine-Dalgarno sequence, suggesting ribosome pausing as the dominant cause of low mutant fitness. Together, our data support the idea that, although a particular set of codons are favored on average across a genome, in an individual gene selection can either act for or against codons depending on their local context.

Population genetic theory predicts that adaptation in novel environments is enhanced by genetic variation for fitness. However, theory also predicts that under strong selection, demographic stochasticity can drive populations to extinction before they can adapt. We exposed wheat-adapted populations of the flour beetle (Tribolium castaneum) to a novel suboptimal corn resource, to test the effects of founding genetic variation on population decline and subsequent extinction or adaptation. As previously Classical population genetic theory predicts that the amount of additive genetic variation for fitness in a population increases the response to directional selection (Fisher 1930). More recent theoretical work suggests, however, that the interaction between genetic variation and fitness is more complex. For instance, the effect of genetic variance in a fitness-relevant trait is also determined by environmental fluctuations, which can inflict a genetic load due to changing phenotypic optima (Lande and Shannon 1996). Another genetic constraint is imposed by the genetic covariance structure, which determines the effect of selection acting simultaneously on multiple traits (Blows and Hoffmann 2005). Additionally, demographic constraints can determine the importance of genetic variation during adaptation. For instance, under

Age-related diseases are often attributed to immunopathology, which results in self-damage caused by an inappropriate inflammatory response. Immunopathology associated with early-life inflammation also appears to cause faster ageing, although we lack direct experimental evidence for this association. To understand the interactions between ageing, inflammation and immunopathology, we used the mealworm beetle as a study organism. We hypothesized that phenoloxidase, an important immune effector in insect defence, may impose substantial immunopathological costs by causing tissue damage to Malpighian tubules (MTs; functionally equivalent to the human kidney), in turn accelerating ageing. In support of this hypothesis, we found that RNAi knockdown of phenoloxidase (PO) transcripts in young adults possibly reduced inflammation-induced autoreactive tissue damage to MTs, and increased adult lifespan. Our work thus suggests a causative link between immunopathological costs of early-life inflammation and faster ageing. We also reasoned that if natural selection weakens with age, older individuals should display increased immunopathological costs associated with an immune response. Indeed, we found that while old infected individuals cleared infection faster than young individuals, possibly they also displayed exacerbated immunopathological costs (larger decline in MT function) and higher post-infection mortality. RNAi-mediated knockdown of PO response partially rescued MTs function in older beetles and resulted in increased lifespan after infection. Taken together, our data are consistent with a direct role of immunopathological consequences of immune response during ageing in insects. Our work is also the first report that highlights the pervasive role of tissue damage under diverse contexts of ageing and immune response.