The red queen coupled with directional selection favours the evolution of sex

Why sexual reproduction has evolved to be such a widespread mode of reproduction remains a major question in evolutionary biology. Although previous studies have shown that increased sex and recombination can evolve in the presence of host-parasite interactions (the 'Red Queen hypothesis' for sex), many of these studies have assumed that multiple loci mediate infection vs. resistance. Data suggest, however, that a major locus is typically involved in antigen presentation and recognition. Here, we explore a model where only one locus mediates host-parasite interactions, but a second locus is subject to directional selection. Even though the effects of these genes on fitness are independent, we show that increased rates of sex and recombination are favoured at a modifier gene that alters the rate of genetic mixing. This result occurs because of selective interference in finite populations (the 'Hill-Robertson effect'), which also favours sex. These results suggest that the Red Queen hypothesis may help to explain the evolution of sex by contributing a form of persistent selection, which interferes with directional selection at other loci and thereby favours sex and recombination.     

Comparative genomics and the study of evolution by natural selection

Genomics profoundly affects most areas of biology, including ecology and evolutionary biology. By examining genome sequences from multiple species, comparative genomics offers new insight into genome evolution and the way natural selection moulds DNA sequence evolution. Functional divergence, as manifested in the accumulation of nonsynonymous substitutions in protein-coding genes, differs among lineages in a manner seemingly related to population size. For example, the ratio of nonsynonymous to synonymous substitution (d_N/d_S) is higher in apes than in rodents, compatible with Ohta's nearly neutral theory of molecular evolution, which suggests that the fixation of slightly deleterious mutations contributes to protein evolution at an extent negatively correlated with effective population size. While this supports the idea that functional evolution is not necessarily adaptive, comparative genomics is uncovering a role for positive Darwinian selection in 10–40% of all genes in different lineages, estimates that are likely to increase when the addition of more genomes gives increased power. Again, population size seems to matter also in this context, with a higher proportion of fixed amino acid changes representing advantageous mutations in large populations. Genes that are particularly prone to be driven by positive selection include those involved with reproduction, immune response, sensory perception and apoptosis. Genetic innovations are also frequently obtained by the gain or loss of complete gene sequences. Moreover, it is increasingly realized, from comparative genomics, that purifying selection conserves much more than just the protein-coding part of the genome, and this points at an important role for regulatory elements in trait evolution. Finally, genome sequencing using outbred or multiple individuals has provided a wealth of polymorphism data that gives information on population history, demography and marker evolution.     

Fertility selection,genetic selection and evolution

The relationship between fertility selection as measured by the correlation in progeny number between parents and offspring, and selection at individual loci is investigated in humans. Estimates for the magnitude of fertility selection (0.1) and the rate of gene substitution (0.5 gene substitutions per generation per genome) are used in various mathematical models for selection. It is found that the observed magnitude of fertility selection cannot be explained by non‐epistatic directional selection at individual loci. A symmetric quantitative directional selection model is consistent with the observed data. But it is possible that fertility selection does not have a genetic basis.     

On the relative roles of faster-X evolution and dominance in the establishment of intrinsic postzygotic isolating barriers

The modern theory of speciation assigns a prominent role to the recessivity of genetic incompatibilities in the two rules of speciation, namely Haldane's rule and the large X effect, and considers that the contribution of faster evolution of the X versus the autosomes to those patterns is generally of relatively minor importance. By extending Turelli and Orr's previous analysis of the model of two-locus Dobzhansky–Muller incompatibilities, I first show that when the X and the autosomes evolve at the same rate, the two dominance parameters involved in that model are not equally important for the declaration of a large X effect, but that the degree of recessivity of homozygous–homozygous incompatibilities is the major determinant for such a declaration. When the X evolves faster than the autosomes, the model obviously predicts that the importance of both dominance parameters will progressively vanish. It is then of importance to obtain estimates of the relative evolutionary rate of X-linked incompatibility loci. Several different procedures to obtain such estimates from the perspective of the large X effect are suggested. The application of the appropriate test to the only suitable data from Drosophila hybridizations so far available leads to the conclusion that the X actually evolves at least 2.5 times faster than the autosomes, as far as hybrid male sterility determinants are concerned, thus making dominance considerations absolutely irrelevant. Notwithstanding the necessity of further tests, the relative roles currently assigned to faster-X evolution and dominance in the theory of speciation should be revised, giving due prominence to faster-X evolution, at least for hybrid male sterility in the genus Drosophila.     

Sporophytic self-incompatibility in Senecio squalidus (Asteraceae): S allele dominance interactions and modifiers of cross-compatibility and selfing rates

Understanding genetic mechanisms of self-incompatibility (SI) and how they evolve is central to understanding the mating behaviour of most outbreeding angiosperms. Sporophytic SI (SSI) is controlled by a single multi-allelic locus, S, which is expressed in the diploid (sporophyte) plant to determine the SI phenotype of its haploid (gametophyte) pollen. This allows complex patterns of independent S allele dominance interactions in male (pollen) and female (pistil) reproductive tissues. Senecio squalidus is a useful model for studying the genetic regulation and evolution of SSI because of its population history as an alien invasive species in the UK. S. squalidus maintains a small number of S alleles (7–11) with a high frequency of dominance interactions. Some S. squalidus individuals also show partial selfing and/or greater levels of cross-compatibility than expected under SSI. We previously speculated that these might be adaptations to invasiveness. Here we describe a detailed characterization of the regulation of SSI in S. squalidus. Controlled crosses were used to determine the S allele dominance hierarchy of six S alleles and effects of modifiers on cross-compatibility and partial selfing. Complex dominance interactions among S alleles were found with at least three levels of dominance and tissue-specific codominance. Evidence for S gene modifiers that increase selfing and/or cross-compatibility was also found. These empirical findings are discussed in the context of theoretical predictions for maintenance of S allele dominance interactions, and the role of modifier loci in the evolution of SI.     

Kin selection and the evolution of sexual conflict

Males and females do not always share the same evolutionary interests. This is particularly true in the case of multiple mating, where male–male competition can often lead to adaptations that are harmful to the female, and females can evolve counter adaptations to reduce the benefits males gain from such traits. Although social evolution has made substantial progress from kin selection theory, most studies of sexual conflict have ignored the effects of genetic relatedness. Here, I use a model of male harm and female resistance to investigate how kin selection affects the evolution of sexual conflict. Building on models of social evolution, I show that relatedness inhibits sexual conflict, in terms of male harm, whereas it has no effect on the evolution female resistance. This study examines a previously neglected mechanism that can potentially help to resolve sexual conflict over mating and highlights the potential importance of considering relatedness in empirical studies of sexual conflict.     

害虫抗药性的显性水平与抗性进化

对杀虫剂的代谢抗性和主要靶标抗性的显性水平作了理论解释,其中包括昆虫对Bt抗性的显性水平的解释。并对抗性显性具有的多变性作了阐述。分析抗性显性水平与抗药性进化的关系,认为在抗性进化早期抗性表现为显性的基因频率上升快于抗性表现为隐性时;但在抗性等位基因频率较高且出现抗性纯合子个体时,抗性表现为隐性的基因频率上升显著快于抗性表现为显性时。最后论述抗性显性在抗性治理中的应用。     

Cultural selection drives the evolution of human communication systems

Human communication systems evolve culturally, but the evolutionary mechanisms that drive this evolution are not well understood. Against a baseline that communication variants spread in a population following neutral evolutionary dynamics (also known as drift models), we tested the role of two cultural selection models: coordination- and content-biased. We constructed a parametrized mixed probabilistic model of the spread of communicative variants in four 8-person laboratory micro-societies engaged in a simple communication game. We found that selectionist models, working in combination, explain the majority of the empirical data. The best-fitting parameter setting includes an egocentric bias and a content bias, suggesting that participants retained their own previously used communicative variants unless they encountered a superior (content-biased) variant, in which case it was adopted. This novel pattern of results suggests that (i) a theory of the cultural evolution of human communication systems must integrate selectionist models and (ii) human communication systems are functionally adaptive complex systems.     

The evolution of genetic canalization under fluctuating selection

Abstract.— If the direction of selection changes from generation to generation, the ability to respond to selection is maladaptive: the response to selection in one generation leads to reduced fitness in the next. Because the response is determined by the amount of genetic variance expressed at the phenotypic level, rapidly fluctuating selection should favor modifier genes that reduce the phenotypic effect of alleles segregating at structural loci underlying the trait. Such reduction in phenotypic expression of genetic variation has been named "genetic canalization." I support this argument with a series of two- and multilocus models with alternating linear selection and Gaussian selection with fluctuating optimum. A canalizing modifier gene affects the fitness of its carriers in three ways: (1) it reduces the phenotypic consequences of genetic response to previous selection; (2) it reduces the genetic response to selection, which is manifested as linkage disequilibrium between the modifier and structural loci; and (3) it reduces the phenotypic variance. The first two effects reduce fitness under directional selection sustained for several generations, but improve fitness when the direction of selection has just been reversed. The net effect tends to favor a canalizing modifier under rapidly fluctuating selection regimes (period of eight generations or less). The third effect improves fitness of the modifier allele if the fitness function is convex and reduces it if the function is concave. Under fluctuating Gaussian selection, the population is more likely to experience the concave portion of the fitness function when selection is stronger. Therefore, only weak to moderately strong fluctuating Gaussian selection favors genetic canalization. This paper considerably broadens the conditions that favor genetic canalization, which so far has only been postulated to evolve under long-term stabilizing selection.     

Positive selection in the evolution of cancer

We hypothesize that forms of antagonistic coevolution have forged strong links between positive selection at the molecular level and increased cancer risk. By this hypothesis, evolutionary conflict between males and females, mothers and foetuses, hosts and parasites, and other parties with divergent fitness interests has led to rapid evolution of genetic systems involved in control over fertilization and cellular resources. The genes involved in such systems promote cancer risk as a secondary effect of their roles in antagonistic coevolution, which generates evolutionary disequilibrium and maladaptation. Evidence from two sources: (1) studies on specific genes, including SPANX cancer/testis antigen genes, several Y-linked genes, the pem homebox gene, centromeric histone genes, the breast cancer gene BRCA1, the angiogenesis gene ANG, cadherin genes, cytochrome P450 genes, and viral oncogenes; and (2) large-scale database studies of selection on different functional categories of genes, supports our hypothesis. These results have important implications for understanding the evolutionary underpinnings of cancer and the dynamics of antagonistically-coevolving molecular systems.     

The evolution of genetic architecture under frequency-dependent disruptive selection

We propose a model to analyze a quantitative trait under frequency-dependent disruptive selection. Selection on the trait is a combination of stabilizing selection and intraspecific competition, where competition is maximal between individuals with equal phenotypes. In addition, there is a density-dependent component induced by population regulation. The trait is determined additively by a number of biallelic loci, which can have different effects on the trait value. In contrast to most previous models, we assume that the allelic effects at the loci can evolve due to epistatic interactions with the genetic background. Using a modifier approach, we derive analytical results under the assumption of weak selection and constant population size, and we investigate the full model by numerical simulations. We find that frequency-dependent disruptive selection favors the evolution of a highly asymmetric genetic architecture, where most of the genetic variation is concentrated on a small number of loci. We show that the evolution of genetic architecture can be understood in terms of the ecological niches created by competition. The phenotypic distribution of a population with an adapted genetic architecture closely matches this niche structure. Thus, evolution of the genetic architecture seems to be a plausible way for populations to adapt to regimes of frequency-dependent disruptive selection. As such, it should be seen as a potential evolutionary pathway to discrete polymorphisms and as a potential alternative to other evolutionary responses, such as the evolution of sexual dimorphism or assortative mating.     

Population structure, levels of selection, and the evolution of intracellular symbionts

Many obligately intracellular symbionts exhibit a characteristic set of genetic changes that include an increase in substitution rates, loss of many genes, and apparent destabilization of many proteins and structural RNAs. Authors have suggested that these changes are due to increased mutation rates, or, more commonly, decreased effective population size due to population bottlenecks at the symbiont or, perhaps, host level. I propose that the increase in substitution rates and accumulation of deleterious mutations is a consequence of the population structure imposed on the endosymbionts by strict host association, loss of horizontal transmission and potentially conflicting levels of selection. I analyze a population genetic model of endosymbiont evolution, and demonstrate that substitution rates will increase, and the effect of those substitutions on endosymbiont fitness will become more deleterious as horizontal transmission among hosts decreases. Additionally, I find that there is a critical level of horizontal transmission below which natural selection cannot effectively purge deleterious mutations, leading to an expected loss of fitness over time. This critical level varies across loci with the degree of correlation between host and endosymbiont fitness, and may help explain differential retention and loss of certain genes.     

Sexual selection expedites the evolution of pesticide resistance

The evolution of insecticide resistance by crop pests and disease vectors causes serious problems for agriculture and health. Sexual selection can accelerate or hinder adaptation to abiotic challenges in a variety of ways, but the effect of sexual selection on resistance evolution is little studied. Here, we examine this question using experimental evolution in the pest insect Tribolium castaneum. The experimental removal of sexual selection slowed the evolution of resistance in populations treated with pyrethroid pesticide, and also reduced the rate at which resistance was lost from pesticide‐free populations. These results suggest that selection arising from variance in mating and fertilization success can augment natural selection on pesticide resistance, meaning that sexual selection should be considered when designing strategies to limit the evolution of pesticide resistance.     

Biological response modifiers (BRM) as antigens

In order to investigate tumoricidal effector cells in therapy by biological response modifiers (BRM) such asPropionibacterium acnes, bacillus Calmette-Guérin (BCG),Streptococcus pyogenes and a protein-bound polysaccharide (PSK), we established T cell lines specific for each BRM from BALB/c mice immunized with the corresponding BRM. These T cell lines proliferated and produced interleukin-2-(IL-2) and/or IL-4, but only in the presence of the relevant BRM and BALB/c spleen cells as the antigen and antigen-presenting cells respectively. Cross-functional experiments indicated that each BRM acts as a nominal antigen, but not as a non-specific immunostimulator. In addition, the T cell lines killed Ia-positive syngeneic B lymphoma cells, but only in the presence of the relevant BRM. These experiments excluded the possibility of cytotoxic effects by each BRM. The T cell lines and clones also killed Ia-negative bystander target cells, but only in the presence of both a relevant antigen and antigen-presenting cells. The T cell clones specific forS. pyogenes orP. acnes tested were Thy1⁺, L3T4⁺ and Lyt2^–. These results indicate that some BRM exert tumoricidal activity by inducing T cells that recognize them as an antigen and kill tumor cells in an antigen-specific manner. The T cells killed tumor targets in either a tumor-necrosis-factor(TNF)-dependent or a TNF-independent manner. The mediator of the latter pathway remains to be elucidated.     

REVIEW: Optimality models in the age of experimental evolution and genomics

Optimality models have been used to predict evolution of many properties of organisms. They typically neglect genetic details, whether by necessity or design. This omission is a common source of criticism, and although this limitation of optimality is widely acknowledged, it has mostly been defended rather than evaluated for its impact. Experimental adaptation of model organisms provides a new arena for testing optimality models and for simultaneously integrating genetics. First, an experimental context with a well‐researched organism allows dissection of the evolutionary process to identify causes of model failure – whether the model is wrong about genetics or selection. Second, optimality models provide a meaningful context for the process and mechanics of evolution, and thus may be used to elicit realistic genetic bases of adaptation – an especially useful augmentation to well‐researched genetic systems. A few studies of microbes have begun to pioneer this new direction. Incompatibility between the assumed and actual genetics has been demonstrated to be the cause of model failure in some cases. More interestingly, evolution at the phenotypic level has sometimes matched prediction even though the adaptive mutations defy mechanisms established by decades of classic genetic studies. Integration of experimental evolutionary tests with genetics heralds a new wave for optimality models and their extensions that does not merely emphasize the forces driving evolution.     

Variability selection in hominid evolution

Variability selection (abbreviated as VS) is a process considered to link adaptive change to large degrees of environment variability. Its application to hominid evolution is based, in part, on the pronounced rise in environmental remodeling that took place over the past several million years. The VS hypothesis differs from prior views of hominid evolution, which stress the consistent selective effects associated with specific habitats or directional trends (e.g., woodland, savanna expansion, cooling). According to the VS hypothesis, wide fluctuations over time created a growing disparity in adaptive conditions. Inconsistency in selection eventually caused habitat-specific adaptations to be replaced by structures and behaviors responsive to complex environmental change. Key hominid adaptations, in fact, emerged during times of heightened variability. Early bipedality, encephalized brains, and complex human sociality appear to signify a sequence of VS adaptations—i.e., a ratcheting up of versatility and responsiveness to novel environments experienced over the past 6 million years. The adaptive results of VS cannot be extrapolated from selection within a single environmental shift or relatively stable habitat. If some complex traits indeed require disparities in adaptive setting (and relative fitness) in order to evolve, the VS idea counters the prevailing view that adaptive change necessitates long-term, directional consistency in selection. © 1998 Wiley-Liss, Inc.     

The robustness of the weak selection approximation for the evolution of altruism against strong selection

The weak selection approximation of population genetics has made possible the analysis of social evolution under a considerable variety of biological scenarios. Despite its extensive usage, the accuracy of weak selection in predicting the emergence of altruism under limited dispersal when selection intensity increases remains unclear. Here, we derive the condition for the spread of an altruistic mutant in the infinite island model of dispersal under a Moran reproductive process and arbitrary strength of selection. The simplicity of the model allows us to compare weak and strong selection regimes analytically. Our results demonstrate that the weak selection approximation is robust to moderate increases in selection intensity and therefore provides a good approximation to understand the invasion of altruism in spatially structured population. In particular, we find that the weak selection approximation is excellent even if selection is very strong, when either migration is much stronger than selection or when patches are large. Importantly, we emphasize that the weak selection approximation provides the ideal condition for the invasion of altruism, and increasing selection intensity will impede the emergence of altruism. We discuss that this should also hold for more complicated life cycles and for culturally transmitted altruism. Using the weak selection approximation is therefore unlikely to miss out on any demographic scenario that lead to the evolution of altruism under limited dispersal.     

Natural selection in chemical evolution

We propose that chemical evolution can take place by natural selection if a geophysical process is capable of heterotrophic formation of liposomes that grow at some base rate, divide by external agitation, and are subject to stochastic chemical avalanches, in the absence of nucleotides or any monomers capable of modular heredity. We model this process using a simple hill-climbing algorithm, and an artificial chemistry that is unique in exhibiting conservation of mass and energy in an open thermodynamic system. Selection at the liposome level results in the stabilization of rarely occurring molecular autocatalysts that either catalyse or are consumed in reactions that confer liposome level fitness; typically they contribute in parallel to an increasingly conserved intermediary metabolism. Loss of competing autocatalysts can sometimes be adaptive. Steady-state energy flux by the individual increases due to the energetic demands of growth, but also of memory, i.e. maintaining variations in the chemical network. Self-organizing principles such as those proposed by Kauffman, Fontana, and Morowitz have been hypothesized as an ordering principle in chemical evolution, rather than chemical evolution by natural selection. We reject those notions as either logically flawed or at best insufficient in the absence of natural selection. Finally, a finite population model without elitism shows the practical evolutionary constraints for achieving chemical evolution by natural selection in the lab.     

Sexual selection and the adaptive evolution of mammalian ejaculate proteins

An elevated rate of substitution characterizes the molecular evolution of reproductive proteins from a wide range of taxa. Although the selective pressures explaining this rapid evolution are yet to be resolved, recent evidence implicates sexual selection as a potentially important explanatory factor. To investigate this hypothesis, we sought evidence of a high rate of adaptive gene evolution linked to postcopulatory sexual selection in muroid rodents, a model vertebrate group displaying a broad range of mating systems. Specifically, we sequenced 7 genes from diverse rodents that are expressed in the testes, prostate, or seminal vesicles, products of which have the potential to act in sperm competition. We inferred positive Darwinian selection in these genes by estimation of the ratio of nonsynonymous (d(N), amino acid changing) to synonymous (d(S), amino acid retaining) substitution rates (omega = d(N)/d(S)). Next, we tested whether variation in this ratio among lineages could be attributed to interspecific variation in mating systems, as inferred from the variation in these rodents' relative testis sizes (RTS). Four of the 7 genes examined (Prm1, Sva, Acrv1, and Svs2, but not Svp2, Msmb, or Spink3) exhibit unambiguous evidence of positive selection. One of these, the seminal vesicle-derived protein Svs2, also shows some evidence for a concentration of positive selection in those lineages in which sperm competition is common. However, this was not a general trend among all the rodent genes we examined. Using the same methods, we then reanalyzed previously published data on 2 primate genes, SEMG1 and SEMG2. Although SEMG2 also shows evidence of positive selection concentrated in lineages subject to high levels of sperm competition, no such trend was found for SEMG1. Overall, despite a high rate of positive selection being a feature of many ejaculate proteins, these results indicate that the action of sexual selection potentially responsible for elevated evolutionary rates may be difficult to detect on a gene-by-gene basis. Although the extreme diversity of reproductive phenotypes exhibited in nature attests to the power of sexual selection, the extent to which this force predominates in driving the rapid molecular evolution of reproductive genes therefore remains to be determined.