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Speciation is less likely to occur when there is gene flow between nascent species. Natural selection can oppose gene flow and promote speciation if there is variation in ecological conditions among the nascent species' locations. Previous theory on ecological speciation with gene flow has focused primarily on the role of genetic variation in ecological traits, largely neglecting the role of nongenetic inheritance or transgenerational plasticity. Here, we build and analyze models incorporating both genetic and epigenetic inheritance, the latter representing a form of nongenetic inheritance. We investigate the rate of speciation for a population that inhabits two patches connected by migration, and find that adaptively biased epigenetic induction can speed up or slow down speciation, depending on the form of the map from genotype and epigenotype to phenotype. While adaptively relevant epigenetic variation can speed up speciation by reducing the fitness of migrants and hybrids, it can also slow down speciation. This latter effect occurs when the epialleles are able to achieve adaptation faster than the genetic alleles, thereby weakening selection on the latter., (© 2022 The Authors. Evolution published by Wiley Periodicals LLC on behalf of The Society for the Study of Evolution.)

Rapid environmental changes are putting numerous species at risk of extinction. For migration-limited species, persistence depends on either phenotypic plasticity or evolutionary adaptation (evolutionary rescue). Current theory on evolutionary rescue typically assumes linear environmental change. Yet accelerating environmental change may pose a bigger threat. Here, we present a model of a species encountering an environment with accelerating or decelerating change, to which it can adapt through evolution or phenotypic plasticity (within-generational or transgenerational). We show that unless either form of plasticity is sufficiently strong or adaptive genetic variation is sufficiently plentiful, accelerating or decelerating environmental change increases extinction risk compared to linear environmental change for the same mean rate of environmental change.

Transgenerational plasticity (TGP) occurs when offspring exhibit plasticity in traits induced by the environments experienced by their parents, and represents a nongenetic mechanism of inheritance. Evidence that traits can be transmitted to future generations by means other than genetic inheritance has caused a surge of interest in epigenetic inheritance, but evidence for epigenetic modifications being both adaptive and heritable remains scarce. What features would make a species most prone to evolve a system of epigenetically mediated adaptive TGP? Here, we use population-genetic models modified to include epigenetic induction and inheritance to investigate if and when epigenetically mediated adaptive TGP would be expected to evolve for a population subdivided between two habitats connected by migration. We show that differences in the direction of selection between the two habitats drives the evolution of epigenetically mediated adaptive TGP. With low migration, the strength of indirect selection in favor of epigenetically mediated adaptive TGP increases with migration rate. Yet, with higher migration, the opposite trend is observed. We predict that species subdivided between habitats that differ in the direction of selection with moderate migration rates between the habitats would be most likely to evolve epigenetically mediated adaptive TGP if costs of producing such systems are not too high., (© 2018 The Author(s). Evolution © 2018 The Society for the Study of Evolution.)

Predators may be limited in their ability to kill prey (i.e., have type II or III functional responses), an insight that has had far-reaching consequences in the ecological literature. With few exceptions, however, this possibility has not been extended to the behaviour of immune cells, which kill pathogens much as predators kill their prey. Rather, models of the within-host environment have tended to tacitly assume that immune cells have an unlimited ability to target and kill pathogens (i.e., a type I functional response). Here we explore the effects of changing this assumption on infection outcomes (i.e., pathogen loads). We incorporate immune cell handling time into an ecological model of the within-host environment that considers both the predatory nature of the pathogen-immune cell interaction as well as competition between immune cells and pathogens for host resources. Unless pathogens can preempt immune cells for host resources, adding an immune cell handling time increases equilibrium pathogen load. We find that the shape of the relationship between energy intake and pathogen load can change: with a type I functional response, pathogen load is maximised at intermediate inputs, while for a type II or III functional response, pathogen load is solely increasing. With a type II functional response, pathogen load can fluctuate rather than settling to an equilibrium, a phenomenon unobserved with type I or III functional responses. Our work adds to a growing literature highlighting the role of resource availability in host-parasite interactions. Implications of our results for adaptive anorexia are discussed., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

The risk of antibiotic resistance evolution in parasites is a major problem for public health. Identifying factors which promote antibiotic resistance evolution is thus a priority in evolutionary medicine. The rate at which new mutations enter the parasite population is one important predictor; however, mutation rate is not necessarily a fixed quantity, as is often assumed, but can itself evolve. Here we explore the possible impacts of mutation rate evolution on the fate of a disease circulating in a host population, which is being treated with drugs, the use of which varies over time. Using an evolutionary rescue framework, we find that mutation rate evolution provides a dramatic increase in the probability that a parasite population survives treatment in only a limited region, while providing little or no advantage in other regions. Both epidemiological features, such as the virulence of infection, and population genetic parameters, such as recombination rate, play important roles in determining the probability of evolutionary rescue and whether mutation rate evolution enhances the probability of evolutionary rescue or not. While efforts to curtail mutation rate evolution in parasites may be worthwhile under some circumstances, our results suggest that this need not always be the case., (Copyright © 2017 Elsevier Inc. All rights reserved.)

The theory that coevolving hosts and parasites create a fluctuating selective environment for one another (i.e., produce Red Queen dynamics) has deep roots in evolutionary biology; yet empirical evidence for Red Queen dynamics remains scarce. Fluctuating coevolutionary dynamics underpin the Red Queen hypothesis for the evolution of sex, as well as hypotheses explaining the persistence of genetic variation under sexual selection, local parasite adaptation, the evolution of mutation rate, and the evolution of nonrandom mating. Coevolutionary models that exhibit Red Queen dynamics typically assume that hosts and parasites encounter one another randomly. However, if related individuals aggregate into family groups or are clustered spatially, related hosts will be more likely to encounter parasites transmitted by genetically similar individuals. Using a model that incorporates familial parasite transmission, we show that a slight degree of familial parasite transmission is sufficient to halt coevolutionary fluctuations. Our results predict that evidence for Red Queen dynamics, and its evolutionary consequences, are most likely to be found in biological systems in which hosts and parasites mix mainly at random, and are less likely to be found in systems with familial aggregation. This presents a challenge to the Red Queen hypothesis and other hypotheses that depend on coevolutionary cycling., (© 2016 The Author(s). Evolution © 2016 The Society for the Study of Evolution.)

Some species mate nonrandomly with respect to alleles underlying immunity. One hypothesis proposes that this is advantageous because nonrandom mating can lead to offspring with superior parasite resistance. We investigate this hypothesis, generalizing previous models in four ways: First, rather than only examining invasibility of modifiers of nonrandom mating, we identify evolutionarily stable strategies. Second, we study coevolution of both haploid and diploid hosts and parasites. Third, we allow for maternal parasite transmission. Fourth, we allow for many alleles at the interaction locus. We find that evolutionarily stable rates of assortative or disassortative mating are usually near zero or one. However, for one case, in which assumptions most closely match the major histocompatibility complex (MHC) system, intermediate rates of disassortative mating can evolve. Across all cases, with haploid hosts, evolution proceeds toward complete disassortative mating, whereas with diploid hosts either assortative or disassortative mating can evolve. Evolution of nonrandom mating is much less affected by the ploidy of parasites. For the MHC case, maternal transmission of parasites, because it creates an advantage to producing offspring that differ from their parents, leads to higher evolutionarily stable rates of disassortative mating. Lastly, with more alleles at the interaction locus, disassortative mating evolves to higher levels., (© 2014 The Author(s). Evolution © 2014 The Society for the Study of Evolution.)

Explaining patterns of diversity has long been a central focus in ecology. One of the most challenging problems has been to understand how species occupying similar ecological niches can co-exist because, with limited resources, demographic stochasticity is expected to lead to the eventual extinction of all but one of them. The Allee effect has been widely studied for its impact on the extinction risk of rare species. Its potential role in promoting co-existence has received less attention. Here, we present a model in which two species compete for a single resource across a continuous landscape. We show that Allee effects can promote their co-existence when a simple condition is met: resources are distributed unevenly across space. Furthermore, the Allee effect can stabilize co-existence despite the reduction in population density and consequent increase in demographic stochasticity that it causes. The Allee effect might, therefore, be an important force maintaining diverse communities., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

By constantly selecting for novel genotypes, coevolution between hosts and parasites can favour elevated mutation rates. Models of this process typically assume random encounters. However, offspring are often more likely to encounter their mother's parasites. Because parents and offspring are genetically similar, they may be susceptible to the same parasite strains and thus, in hosts, maternal transmission should select for mechanisms that decrease intergenerational genetic similarity. In parasites, however, maternal transmission should select for genetic similarity. We develop and analyse a model of host and parasite mutation rate evolution when parasites are maternally inherited. In hosts, we find that maternal transmission has two opposing effects. First, it eliminates coevolutionary cycles that previous work shows select for higher mutation. Second, it independently selects for higher mutation rates, because offspring that differ from their mothers are more likely to avoid infection. In parasites, however, the two effects of maternal transmission act in the same direction. As for hosts, maternal transmission eliminates coevolutionary cycles, thereby reducing selection for increased mutation. Unlike for hosts, however, maternal transmission additionally selects against higher mutation by favouring parasite offspring that are the same as their mothers.

Since its discovery in 1907, polyploidy has been recognized as an important phenomenon in vascular plants, and several lines of evidence indicate that most, if not all, plant species ultimately have a polyploid ancestry. However, previous estimates of the frequency of polyploid speciation suggest that the formation and establishment of neopolyploid species is rare. By combining information from the botanical community's vast cytogenetic and phylogenetic databases, we establish that 15% of angiosperm and 31% of fern speciation events are accompanied by ploidy increase. These frequency estimates are higher by a factor of four than earlier estimates and lead to a standing incidence of polyploid species within genera of 35% (n = 1,506). Despite this high incidence, we find no direct evidence that polyploid lines, once established, enjoy greater net species diversification. Thus, the widespread occurrence of polyploid taxa appears to result from the substantial contribution of polyploidy to cladogenesis, but not from subsequent increases in diversification rates of polyploid lines.

Most models of Fisherian sexual selection assume haploidy. However, analytical models that focus on dynamics near fixation boundaries and simulations show that the resulting behavior depends on ploidy. Here we model sexual selection in a diploid to characterize behaviour away from fixation boundaries. The model assumes two di-allelic loci, a male-limited trait locus subject to viability selection, and a preference locus that determines a female's tendency to mate with males based on their genotype at the trait locus. Using a quasi-linkage equilibrium (QLE) approach, we find a general equation for the curves of quasi-neutral equilibria, and the conditions under which they are attracting or repelling. Unlike in the haploid model, the system can move away from the internal curve of equilibria in the diploid model. We show that this is the case when the combined forces of natural and sexual selection induce underdominance at the trait locus.