Why isn’t random variation always deleterious? Are there factors that sometimes make adaptation easier? Biological systems are extraordinarily robust to perturbation by mutations, recombination, and the environment. It has been proposed that this robustness might make them more evolvable. Robustness to mutation allows genetic variation to accumulate in a cryptic state. Switching mechanisms known as evolutionary capacitors mean that the amount of heritable phenotypic variation available can be correlated to the degree of stress and hence to the novelty of the environment and remaining potential for adaptation. There have been two somewhat separate literatures relating robustness to evolvability. One has focused on molecular phenotypes and new mutations, the other on morphology and cryptic genetic variation. Here we review both literatures, and show that the true distinction is whether recombination rates are high or low. In both cases, the evidence supports the claim that robustness promotes evolvability.

In the past six decades, lifespan inequality has varied greatly within and among countries even while life expectancy has continued to increase. How and why does mortality change generate this diversity? We derive a precise link between changes in age-specific mortality and lifespan inequality, measured as the variance of age at death. Key to this relationship is a young–old threshold age, below and above which mortality decline respectively decreases and increases lifespan inequality. First, we show for Sweden that shifts in the threshold’s location have modified the correlation between changes in life expectancy and lifespan inequality over the last two centuries. Second, we analyze the post–World War II (WWII) trajectories of lifespan inequality in a set of developed countries—Japan, Canada, and the United States—where thresholds centered on retirement age. Our method reveals how divergence in the age pattern of mortality change drives international divergence in lifespan inequality. Most strikingly, early in the 1980s, mortality increases in young U.S. males led to a continuation of high lifespan inequality in the United States; in Canada, however, the decline of inequality continued. In general, our wider international comparisons show that mortality change varied most at young working ages after WWII, particularly for males. We conclude that if mortality continues to stagnate at young ages yet declines steadily at old ages, increases in lifespan inequality will become a common feature of future demographic change. Keywords Disparity, Health, Longevity, Retirement, Social policy

We examined how ecological and evolutionary (eco-evo) processes in population dynamics could be better integrated into population viability analysis (PVA). Complementary advances in computation and population genomics can be combined into an eco-evo PVA to offer powerful new approaches to understand the influence of evolutionary processes on population persistence. We developed the mechanistic basis of an eco-evo PVA using individual-based models with individual-level genotype tracking and dynamic genotype-phenotype mapping to model emergent population-level effects, such as local adaptation and genetic rescue. We then outline how genomics can allow or improve parameter estimation for PVA models by providing genotypic information at large numbers of loci for neutral and functional genome regions. As climate change and other threatening processes increase in rate and scale, eco-evo PVAs will become essential research tools to evaluate the effects of adaptive potential, evolutionary rescue, and locally adapted traits on persistence.

When individuals' fitnesses depend on the genetic composition of the population in which they are found, selection is then frequency dependent. Frequency-dependent selection (FDS) is often invoked as a heuristic explanation for the maintenance of large numbers of alleles at a locus. The pairwise interaction model is a general model of FDS via intraspecific competition at the genotypic level. Here we use a parameter-space approach to investigate the full potential for the maintenance of multiallelic equilibria under the pairwise interaction model. We find that FDS maintains full polymorphism more often than classic constant-selection models and produces more skewed equilibrium allele frequencies. Fitness sets with some degree of rare advantage maintained full polymorphism most often, but a wide variety of nonobvious fitness patterns were also found to have positive potential for polymorphism. An example is put forth suggesting possible explanations for multiallelic polymorphisms maintained despite positive FDS on individual alleles.