Incorporating evolutionary processes into population viability models.

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.

Deciphering life history transcriptomes in different environments.

We compared whole transcriptome variation in six pre-adult stages and seven adult female ages in two populations of cactophilic Drosophila mojavensis reared on two host plants to understand how differences in gene expression influence standing life history variation. We used singular value decomposition (SVD) to identify dominant trajectories of life cycle gene expression variation, performed pairwise comparisons of stage and age differences in gene expression across the life cycle, identified when genes exhibited maximum levels of life cycle gene expression, and assessed population and host cactus effects on gene expression. Life cycle SVD analysis returned four significant components of transcriptional variation, revealing functional enrichment of genes responsible for growth, metabolic function, sensory perception, neural function, translation and ageing.

Cryptic genetic variation can make "irreducible complexity" a common mode of adaptation in sexual populations.

The existence of complex (multiple-step) genetic adaptations that are "irreducible" (i.e., all partial combinations are less fit than the original genotype) is one of the longest standing problems in evolutionary biology.

Divergence in age patterns of mortality change drives international divergence in lifespan inequality.

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.

Birth-order differences can drive natural selection on aging.

Senescence-the deterioration of survival and reproductive capacity with increasing age-is generally held to be an evolutionary consequence of the declining strength of natural selection with increasing age. The diversity in rates of aging observed in nature suggests that the rate at which age-specific selection weakens is determined by species-specific ecological factors. We propose that, in iteroparous species, relationships between parental age, offspring birth order, and environment may affect selection on senescence.

Models of frequency-dependent selection with mutation from parental alleles.

Frequency-dependent selection (FDS) remains a common heuristic explanation for the maintenance of genetic variation in natural populations. The pairwise-interaction model (PIM) is a well-studied general model of frequency-dependent selection, which assumes that a genotype's fitness is a function of within-population intergenotypic interactions. Previous theoretical work indicated that this type of model is able to sustain large numbers of alleles at a single locus when it incorporates recurrent mutation.

Beyond the Mean: Sensitivities of the Variance of Population Growth.

Populations in variable environments are described by both a mean growth rate and a variance of stochastic population growth. Increasing variance will increase the width of confidence bounds around estimates of population size, growth, probability of and time to quasi-extinction. However, traditional sensitivity analyses of stochastic matrix models only consider the sensitivity of the mean growth rate.

Robustness and evolvability.

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.

Complex dynamics occur in a single-locus, multiallelic model of general frequency-dependent selection.

We examine the characteristics of non-equilibrium dynamics produced by a simple well-known model of frequency-dependent selection at a single diploid locus. An examination of the parameter space of this "pairwise-interaction model" (PIM) revealed non-equilibrium dynamics for polymorphisms of 3, 4 and 5 alleles; both allele-frequency cycling and aperiodic trajectories were detected. We measured the number, cycle length and domains of attraction of the various attractors produced by the model.

The generation and maintenance of genetic variation by frequency-dependent selection: constructing polymorphisms under the pairwise interaction model.

Frequency-dependent selection remains the most commonly invoked heuristic explanation for the maintenance of genetic variation. For polymorphism to exist, new alleles must be both generated and maintained in the population. Here we use a construction approach to model frequency-dependent selection with mutation under the pairwise interaction model.

Evolution of fitnesses in structured populations with correlated environments.

The outcome of selection in structured populations with spatially varying selection pressures depends on the interaction of two factors: the level of gene flow and the amount of heterogeneity among the demes. Here we investigate the effect of three different levels of spatial heterogeneity on the levels of genetic polymorphisms for different levels of gene flow, using a construction approach in which a population is constantly bombarded with new mutations. We further compare the relative importance of two kinds of balancing selection (heterozygote advantage and selection arising from spatial heterogeneity), the level of adaptation and the stability of the resulting polymorphic equilibria.

Frequency-dependent selection and the maintenance of genetic variation: exploring the parameter space of the multiallelic pairwise interaction model.

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.