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The problem of whether haplodiploidy is responsible for the frequent evolution of eusociality in the Hymenoptera remains unresolved. The little-known "protected invasion hypothesis" posits that because a male will transmit a new allele for alloparental care to all his daughters under haplodiploidy, such an allele has a higher probability of spreading to fixation under haplodiploidy than under diploidy. This mechanism is investigated using the mating system and lifecycles ancestral to eusocial lineages. It is shown that although haplodiploidy increases the probability of fixation of a new allele, the effect is cancelled by a higher probability of the allele arising in a diploid population. However, the same effect of male haploidy results in a 30% lower threshold amount of reproductive help by a worker necessary to favor eusociality if the sex ratio of dispersing first-brood offspring remains even. This occurs because when first-brood daughters become workers, the sex ratio of dispersing first-brood offspring becomes male-biased, selecting for an overall female-biased first-brood sex ratio. Through this mechanism, haplodiploidy may favor eusociality in the absence of a female-biased sex ratio in dispersing reproductive offspring. The gene-centric approach used here reveals the critical role of male haploidy in structuring the social group.

The disruptive selection theory of the evolution of anisogamy posits that the evolution of a larger body or greater organismal complexity selects for a larger zygote, which in turn selects for larger gametes. This may provide the opportunity for one mating type to produce more numerous, small gametes, forcing the other mating type to produce fewer, large gametes. Predictions common to this and related theories have been partially upheld. Here, a prediction specific to the disruptive selection theory is derived from a previously published game‐theoretic model that represents the most complete description of the theory. The prediction, that the ratio of macrogamete to microgamete size should be above three for anisogamous species, is supported for the volvocine algae. A fully population genetic implementation of the model, involving mutation, genetic drift, and selection, is used to verify the game‐theoretic approach and accurately simulates the evolution of gamete sizes in anisogamous species. This model was extended to include a locus for gamete motility and shows that oogamy should evolve whenever there is costly motility. The classic twofold cost of sex may be derived from the fitness functions of these models, showing that this cost is ultimately due to genetic conflict.

Pathogens adapt to antibody surveillance through amino acid replacements in targeted protein regions, or epitopes, that interfere with antibody binding. However, such escape mutations may exact a fitness cost due to impaired protein function. Here, it is hypothesized that the recurring generation of specific neutralizing antibodies to an epitope region as it evolves in response to antibody selection will cause amino acid reversions by releasing early escape mutations from immune selection. The plausibility of this hypothesis was tested with stochastic simulation of adaptation at the molecular sequence level in finite populations. Under the conditions of strong selection and weak mutation, the rates of allele fixation and amino acid reversion increased with population size and selection coefficients. These rates decreased with population size, however, if mutation became strong, because clonal interference reduced the rate of adaptation. The model successfully predicts the rate of reversion per allele fixation for an important human immunodeficiency virus type 1 (HIV-1) antibody epitope region. Therefore, antibody selection may generate complex adaptive dynamics.

The mutational landscape model of adaptive sequence evolution has been used to explain an unexpected strong positive linear relationship between marginal fitness and mean site-specific amino acid frequency in the functionally important HIV-1 gp120 V3 protein region. The model predicts a positive linear relationship between the probability that a particular beneficial allele, among several, is the next to spread to fixation during an adaptive walk, its transition probability, and the allele's selection coefficient. Here, stochastic simulation is used to confirm the intuition that the linear relationship between transition probabilities and selection coefficients, predicted by the model, should, under fluctuating selection, produce a linear relationship between allele frequency, averaged across populations, and fitness. In addition, these relationships hold for the effective population size and mutation rate of HIV-1 and for the moderately strong selection observed for V3. A survey of the strength of mutation for diverse organisms suggests that these relationships may be widely applicable.