Heterosis in age‐specific selected populations of a seed beetle: Sex differences in longevity and reproductive behavior

We tested mutation accumulation hypothesis for the evolution of senescence using short‐lived and long‐lived populations of the seed‐feeding beetle, Acanthoscelides obtectus (Say), obtained by selection on early‐ and late‐life for many generations. The expected consequence of the mutation accumulation hypothesis is that in short‐lived populations, where the force of natural selection is the strongest early in life, the late‐life fitness traits should decline due to genetic drift which increases the frequency of mutations with deleterious effects in later adult stages. Since it is unlikely that identical deleterious mutations will increase in several independent populations, hybrid vigor for late‐life fitness is expected in offspring obtained in crosses among populations selected for early‐life fitness traits. We tested longevity of both sexes, female fecundity and male reproductive behavior for hybrid vigor by comparing hybrid and nonhybrid short‐lived populations. Hybrid vigor was confirmed for male virility, mating speed and copulation duration, and longevity of both sexes at late ages. In contrast to males, the results on female fecundity in short‐lived populations did not support mutation accumulation as a genetic mechanism for the evolution of this trait. Contrary to the prediction of this hypothesis, male mating ability indices and female fecundity in long‐lived populations exhibited hybrid vigor at all assayed age classes. We demonstrate that nonhybrid long‐lived populations diverged randomly regarding female and male reproductive fitness, indicating that sexually antagonistic selection, when accompanied with genetic drift for female fecundity and male virility, might be responsible for overriding natural selection in the independently evolving long‐lived populations.     

Implications of mate search, mate choice and divorce rate for population dynamics of sexually reproducing species

In this paper we examine how the process of mate search, degree of mate choice and degree of mate fidelity may interact to affect long‐term population dynamics of sexually reproducing species. In particular, we address the following questions: are degree of mate choice and degree of mate fidelity correlated? How does mate search shape this relationship? How does longevity affect mating behaviour? To resolve these questions, we develop a spatially explicit, individual‐based model of a sexually reproducing population with single (i.e. unpaired) males, single females, and pairs as focal individuals. Both this model and its non‐spatial approximation give rise to the Allee effect due to lack of mating possibilities, and sufficiently small/sparse populations always go extinct. We quantify combinations of mate choice and divorce rate under which populations persist or go extinct even from high sizes. We thus show that there exist ecological constraints for possible (co)evolution of mate choice and pair maintenance behaviour. Our models also suggest that colonial species with active mate search strategy survive at higher divorce rates than less colonial animals that search for their mates randomly, and that long‐lived species sustain at higher degrees of mate choice and lower degrees of mate fidelity compared to the short‐lived ones. Connection of these findings to other theoretical results and some empirical observations is discussed.     

Effect of habitat area and isolation on plant trait distribution in European forests and grasslands

A number of studies show contrasting results in how plant species with specific life‐history strategies respond to fragmentation, but a general analysis on whether traits affect plant species occurrences in relation to habitat area and isolation has not been performed. We used published data from forests and grasslands in north‐central Europe to analyse if there are general patterns of sensitivity to isolation and dependency of area for species using three traits: life‐span, clonality, and seed weight. We show that a larger share of all forest species was affected by habitat isolation and area as compared to grassland species. Persistence‐related traits, life‐span and clonality, were associated to habitat area and the dispersal and recruitment related trait, seed weight, to isolation in both forest and grassland patches. Occurrence of clonal plant species decreased with habitat area, opposite to non‐clonal plant species, and long‐lived plant species decreased with grassland area. The directions of these responses partly challenge some earlier views, suggesting that further decrease in habitat area will lead to a change in plant species community composition, towards relatively fewer clonal and long‐lived plants with large seeds in small forest patches and fewer clonal plants with small seeds in small grassland patches. It is likely that this altered community has been reached in many fragmented European landscapes consisting of small and isolated natural and semi‐natural patches, where many non‐clonal and short‐lived species have already disappeared. Our study based on a large‐scale dataset reveals general and useful insights concerning area and isolation effects on plant species composition that can improve the outcome of conservation and restoration efforts of plant communities in rural landscapes.     

Species selection and random drift in macroevolution

Species selection resulting from trait‐dependent speciation and extinction is increasingly recognized as an important mechanism of phenotypic macroevolution. However, the recent bloom in statistical methods quantifying this process faces a scarcity of dynamical theory for their interpretation, notably regarding the relative contributions of deterministic versus stochastic evolutionary forces. I use simple diffusion approximations of birth‐death processes to investigate how the expected and random components of macroevolutionary change depend on phenotype‐dependent speciation and extinction rates, as can be estimated empirically. I show that the species selection coefficient for a binary trait, and selection differential for a quantitative trait, depend not only on differences in net diversification rates (speciation minus extinction), but also on differences in species turnover rates (speciation plus extinction), especially in small clades. The randomness in speciation and extinction events also produces a species‐level equivalent to random genetic drift, which is stronger for higher turnover rates. I then show how microevolutionary processes including mutation, organismic selection, and random genetic drift cause state transitions at the species level, allowing comparison of evolutionary forces across levels. A key parameter that would be needed to apply this theory is the distribution and rate of origination of new optimum phenotypes along a phylogeny.     

The distribution of mitochondrial DNA heteroplasmy due to random genetic drift

Cells containing pathogenic mutations in mitochondrial DNA (mtDNA) generally also contain the wild-type mtDNA, a condition called heteroplasmy. The amount of mutant mtDNA in a cell, called the heteroplasmy level, is an important factor in determining the amount of mitochondrial dysfunction and therefore the disease severity. mtDNA is inherited maternally, and there are large random shifts in heteroplasmy level between mother and offspring. Understanding the distribution in heteroplasmy levels across a group of offspring is an important step in understanding the inheritance of diseases caused by mtDNA mutations. Previously, our understanding of the heteroplasmy distribution has been limited to just the mean and variance of the distribution. Here we give equations, adapted from the work of Kimura on random genetic drift, for the full mtDNA heteroplasmy distribution. We describe how to use the Kimura distribution in mitochondrial genetics, and we test the Kimura distribution against human, mouse, and Drosophila data sets.     

Fibroblasts from long‐lived species of mammals and birds show delayed,but prolonged,phosphorylation of ERK

Fibroblasts from long‐lived mutant mice show diminished phosphorylation of the stress‐activated protein kinases ERK1/2 after exposure to peroxide, cadmium, or paraquat. We have now evaluated the kinetics of ERK phosphorylation in fibroblasts from long‐lived and short‐lived species of mammals and birds in response to stress by cadmium or hydrogen peroxide. Fibroblasts from the shorter‐lived species of rodents and birds showed rapid induction of ERK phosphorylation, with a decline to basal level within 60 min. In contrast, cells from longer‐lived species showed slower and more prolonged activation of ERK phosphorylation. These results suggest that fibroblasts from long‐lived species may be less susceptible to the early phases of damage from cadmium or peroxide and suggest that altered kinetics of ERK activity may contribute to their stress resistance properties.     

Effects of clonality on the genetic variability of rare,insular species: the case of Ruta microcarpa from the Canary Islands

Many plant species combine sexual and clonal reproduction. Clonal propagation has ecological costs mainly related to inbreeding depression and pollen discounting; at the same time, species able to reproduce clonally have ecological and evolutionary advantages being able to persist when conditions are not favorable for sexual reproduction. The presence of clonality has profound consequences on the genetic structure of populations, especially when it represents the predominant reproductive strategy in a population. Theoretical studies suggest that high rate of clonal propagation should increase the effective number of alleles and heterozygosity in a population, while an opposite effect is expected on genetic differentiation among populations and on genotypic diversity. In this study, we ask how clonal propagation affects the genetic diversity of rare insular species, which are often characterized by low levels of genetic diversity, hence at risk of extinction. We used eight polymorphic microsatellite markers to study the genetic structure of the critically endangered insular endemic Ruta microcarpa. We found that clonality appears to positively affect the genetic diversity of R. microcarpa by increasing allelic diversity, polymorphism, and heterozygosity. Moreover, clonal propagation seems to be a more successful reproductive strategy in small, isolated population subjected to environmental stress. Our results suggest that clonal propagation may benefit rare species. However, the advantage of clonal growth may be only short‐lived for prolonged clonal growth could ultimately lead to monoclonal populations. Some degree of sexual reproduction may be needed in a predominantly clonal species to ensure long‐term viability.     

Random intracellular drift explains the clonal expansion of mitochondrial DNA mutations with age

Human tissues acquire somatic mitochondrial DNA (mtDNA) mutations with age. Very high levels of specific mtDNA mutations accumulate within individual cells, causing a defect of mitochondrial oxidative metabolism. This is a fundamental property of nondividing tissues, but it is not known how it comes about. To explore this problem, we developed a model of mtDNA replication within single human cells. Using this model, we show that relaxed replication of mtDNA alone can lead, through random genetic drift, to the clonal expansion of single mutant events during human life. Significant expansions primarily develop from mutations acquired during a critical period in childhood or early adult life.     

Mathematical Modeling of the Role of Mitochondrial Fusion and Fission in Mitochondrial DNA Maintenance

Accumulation of mitochondrial DNA (mtDNA) mutations has been implicated in a wide range of human pathologies, including neurodegenerative diseases, sarcopenia, and the aging process itself. In cells, mtDNA molecules are constantly turned over (i.e. replicated and degraded) and are also exchanged among mitochondria during the fusion and fission of these organelles. While the expansion of a mutant mtDNA population is believed to occur by random segregation of these molecules during turnover, the role of mitochondrial fusion-fission in this context is currently not well understood. In this study, an in silico modeling approach is taken to investigate the effects of mitochondrial fusion and fission dynamics on mutant mtDNA accumulation. Here we report model simulations suggesting that when mitochondrial fusion-fission rate is low, the slow mtDNA mixing can lead to an uneven distribution of mutant mtDNA among mitochondria in between two mitochondrial autophagic events leading to more stochasticity in the outcomes from a single random autophagic event. Consequently, slower mitochondrial fusion-fission results in higher variability in the mtDNA mutation burden among cells in a tissue over time, and mtDNA mutations have a higher propensity to clonally expand due to the increased stochasticity. When these mutations affect cellular energetics, nuclear retrograde signalling can upregulate mtDNA replication, which is expected to slow clonal expansion of these mutant mtDNA. However, our simulations suggest that the protective ability of retrograde signalling depends on the efficiency of fusion-fission process. Our results thus shed light on the interplay between mitochondrial fusion-fission and mtDNA turnover and may explain the mechanism underlying the experimentally observed increase in the accumulation of mtDNA mutations when either mitochondrial fusion or fission is inhibited.     

Long‐term and contemporary environmental conditions as determinants of the species composition of bog organisms

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Relaxed replication of mtDNA: A model with implications for the expression of disease

Heteroplasmic mtDNA defects are an important cause of human disease with clinical features that primarily involve nondividing (postmitotic) tissues. Within single cells the percentage level of mutated mtDNA must exceed a critical threshold level before the genetic defect is expressed. Although the level of mutated mtDNA may alter over time, the mechanism behind the change is not understood. It currently is not possible to directly measure the level of mutant mtDNA within living cells. We therefore developed a mathematical model of human mtDNA replication, based on a solid foundation of experimentally derived parameters, and studied the dynamics of intracellular heteroplasmy in postmitotic cells. Our simulations show that the level of intracellular heteroplasmy can vary greatly over a short period of time and that a high copy number of mtDNA molecules delays the time to fixation of an allele. We made the assumption that the optimal state for a cell is to contain 100% wild-type molecules. For cells that contain pathogenic mutations, the nonselective proliferation of mutant and wild-type mtDNA molecules further delays the fixation of both alleles, but this leads to a rapid increase in the mean percentage level of mutant mtDNA within a tissue. On its own, this mechanism will lead to the appearance of a critical threshold level of mutant mtDNA that must be exceeded before a cell expresses a biochemical defect. The hypothesis that we present is in accordance with the available data and may explain the late presentation and insidious progression of mtDNA diseases.     

Resource competition and fire‐regulated nutrient demand in carnivorous plants of wet pine savannas

Question: What are the mechanisms by which fire reduces competition for both a short‐lived and a long‐lived species in old‐growth ground‐cover plant communities of wet pine savannas (originally Pinus palustris, replaced by P. elliottii)? Location: Outer coastal plain of southeastern Mississippi, USA. Methods: I reviewed previous competition experiments and proposed a new hypothesis to explain the relationship between fire, competition, and species co‐existence in wet longleaf pine savannas. The first study is about growth and seedling emergence responses of a short‐lived carnivorous plant, Drosera capillaris, to reduction in below‐ground competition and above‐ plus below‐ground competition. The second study deals with growth and survival responses of a long‐lived perennial carnivorous plant, Sarracenia alata, to neighbour removal and prey‐exclusion to determine if a reduction in nutrient supply increased the intensity of competition in this nutrient‐poor system. Results: Fire increased seedling emergence of the short‐lived species by reducing above‐ground competition through the destruction of above‐ground parts of plants and the combustion of associated litter. Prey exclusion did not increase competitive effects of neighbours on the long‐lived species. However, because the experiment was conducted in a year without fire, shade reduced nutrient demand, which may have obviated competition for soil nutrients between Sarracenia alata and its neighbours. Conclusion: Repeated fires likely interact with interspecific differences in nutrient uptake to simultaneously reduce both above‐ground competition and competition for nutrients in old‐growth ground cover communities in pine savannas. Restoration practitioners should consider the possibility that the composition of the plant community is just as important as fire in ensuring that frequent fires maintain species diversity.     

Linking demographic responses and life history tactics from longitudinal data in mammals

In stochastic environments, a change in a demographic parameter can influence the population growth rate directly or via a resulting impact on age structure. Stochastic elasticity of the long‐run stochastic growth rate λ_s to a demographic parameter offers a suitable way to measure the overall demographic response because it includes both the direct effect of changing the demographic parameter and its indirect effect through changes in the age structure. From 25 mammalian populations with contrasting life histories, we investigated how pace of life and population growth rate influence the demographic responses (measured as the relative contributions of the direct and indirect components of stochastic elasticity on λ_s). We found that in short‐lived species, the change in population structure resulting from an increase in yearling survival leads to an additional increase in λ_s, whereas in long‐lived species, the same change in population structure leads to a decrease. Short‐lived species thus display a boom‐bust life history strategy contrary to long‐lived species, for which the long lifespan dampens the demographic consequences of changing age structure. Irrespective of the species’ life history strategy, the change in population age structure resulting from an increase in adult survival leads to an additional increase in λ_s due to an increase of the proportion of mature individuals in the population. On the contrary, a change in population age structure resulting from an increase of reproductive performance leads to a decrease in λ_s that is due to the increase of the proportion of immature individuals in the population. Our comparative analysis of stochastic elasticity patterns in mammals shows the existence of different demographic responses to changes in age structure between short‐ and long‐lived species, which improves our understanding of population dynamics in variable environments in relation to the species‐specific pace of life.     

Fixation probability in a two-locus model by the ancestral recombination-selection graph

We use the ancestral influence graph (AIG) for a two-locus, two-allele selection model in the limit of a large population size to obtain an analytic approximation for the probability of ultimate fixation of a single mutant allele A. We assume that this new mutant is introduced at a given locus into a finite population in which a previous mutant allele B is already segregating with a wild type at another linked locus. We deduce that the fixation probability increases as the recombination rate increases if allele A is either in positive epistatic interaction with B and allele B is beneficial or in no epistatic interaction with B and then allele A itself is beneficial. This holds at least as long as the recombination fraction and the selection intensity are small enough and the population size is large enough. In particular this confirms the Hill-Robertson effect, which predicts that recombination renders more likely the ultimate fixation of beneficial mutants at different loci in a population in the presence of random genetic drift even in the absence of epistasis. More importantly, we show that this is true from weak negative epistasis to positive epistasis, at least under weak selection. In the case of deleterious mutants, the fixation probability decreases as the recombination rate increases. This supports Muller's ratchet mechanism to explain the accumulation of deleterious mutants in a population lacking recombination.     

Weakened purifying selection leads to elevated mutation load under environmental sex determination

In many gonochoristic taxa, sex is influenced by developmental environment, a system that can lead to temporal fluctuations in offspring sex ratio. Demographic models suggest that only short‐lived species with environmental sex determination (ESD) are negatively impacted by sex‐ratio fluctuations, yet these models fail to account for the potential mutation load associated with reductions in genetically effective population sizes. In this study, we developed a series of individual‐based simulation models that explore the fixation rates of mildly deleterious alleles under different sex‐determining systems and examine the impacts of variation in lifespan and offspring sex ratio. Populations with ESD exhibited increases in fixation rates in both short‐ and long‐lived populations, but substantial increases were limited to populations characterized by a combination of high sex‐ratio variation and short lifespan. Fixation rates were negatively associated with effective population size, indicating that purifying selection operates less efficiently under ESD relative to genotypic sex determination. Reductions in effective population size could be attributed to both intragenerational forces (unequal sex ratio) and intergenerational forces (variable census population sizes). Levels of temporal sex‐ratio variation calculated from wild populations of ESD species were capable of yielding large increases in fixation rates, although this relationship was strongly mediated by lifespan. Our results may help to explain the limited phylogenetic distribution of ESD in short‐lived taxa.     

Length Heteroplasmy of Sturgeon Mitochondrial DNA: An Illegitimate Elongation Model

Extensive length polymorphism and heteroplasmy (multiple forms within an individual) of the D-loop region are observed in mitochondrial DNA of the white sturgeon (Acipenser transmontanus). The nucleotide sequence of this region, for both a short and a long form, shows that the differences are due to variable numbers of a perfect 82-bp direct repeat. We propose a model for the replicative origin of length differences, involving a competitive equilibrium between the heavy strand and the D-loop strand. This model suggests that frequent misalignment in the repeat region prior to elongation, facilitated by a stable secondary structure in the displaced strand, can explain both the polymorphism and heteroplasmy in this species.     

Within‐season increase in parental investment in a long‐lived bird species: investment shifts to maximize successful reproduction?

In nest‐building species predation of nest contents is a main cause of reproductive failure and parents have to trade off reproductive investment against antipredatory behaviours. While this trade‐off is modified by lifespan (short‐lived species prioritize current reproduction; long‐lived species prioritize future reproduction), it may vary within a breeding season, but this idea has only been tested in short‐lived species. Yet, life history theory does not make any prediction how long‐lived species should trade off current against future reproductive investment within a season. Here, we investigated this trade‐off through predator‐exposure experiments in a long‐lived bird species, the brown thornbill. We exposed breeding pairs that had no prior within‐season reproductive success to the models of a nest predator and a predator of adults during their first or second breeding attempt. Overall, parents reduced their feeding rate in the presence of a predator, but parents feeding second broods were more risk sensitive and almost ceased feeding when exposed to both types of predators. However, during second breeding attempts, parents had larger clutches and a higher feeding rate in the absence of predators than during first breeding attempts and approached both types of predators closer when mobbing. Our results suggest that the trade‐off between reproductive investment and risk‐taking can change in a long‐lived species within a breeding season depending on both prior nest predation and renesting opportunities. These patterns correspond to those in short‐lived species, raising the question of whether a within‐season shift in reproductive investment trade‐offs is independent of lifespan.     

The Ratchet and the Red Queen: the maintenance of sex in parasites

The adaptive significance of sexual reproduction remains as an unsolved problem in evolutionary biology. One promising hypothesis is that frequency‐dependent selection by parasites selects for sexual reproduction in hosts, but it is unclear whether such selection on hosts would feed back to select for sexual reproduction in parasites. Here we used individual‐based computer simulations to explore this possibility. Specifically, we tracked the dynamics of asexual parasites following their introduction into sexual parasite populations for different combinations of parasite virulence and transmission. Our results suggest that coevolutionary interactions with hosts would generally lead to a stable coexistence between sexual parasites and a single parasite clone. However, if multiple mutations to asexual reproduction were allowed, we found that the interaction led to the accumulation of clonal diversity in the asexual parasite population, which led to the eventual extinction of the sexual parasites. Thus, coevolution with sexual hosts may not be generally sufficient to select for sex in parasites. We then allowed for the stochastic accumulation of mutations in the finite parasite populations (Muller's Ratchet). We found that, for higher levels of parasite virulence and transmission, the population bottlenecks resulting from host–parasite coevolution led to the rapid accumulation of mutations in the clonal parasites and their elimination from the population. This result may explain the observation that sexual reproduction is more common in parasitic animals than in their free‐living relatives.     

No evidence for accumulation of deleterious mutations and fitness degradation in clonal fish hybrids: Abandoning sex without regrets

Despite its inherent costs, sexual reproduction is ubiquitous in nature, and the mechanisms to protect it from a competitive displacement by asexuality remain unclear. Popular mutation‐based explanations, like the Muller's ratchet and the Kondrashov's hatchet, assume that purifying selection may not halt the accumulation of deleterious mutations in the nonrecombining genomes, ultimately leading to their degeneration. However, empirical evidence is scarce and it remains particularly unclear whether mutational degradation proceeds fast enough to ensure the decay of clonal organisms and to prevent them from outcompeting their sexual counterparts. To test this hypothesis, we jointly analysed the exome sequences and the fitness‐related phenotypic traits of the sexually reproducing fish species and their clonal hybrids, whose evolutionary ages ranged from F1 generations to 300 ky. As expected, mutations tended to accumulate in the clonal genomes in a time‐dependent manner. However, contrary to the predictions, we found no trend towards increased nonsynonymity of mutations acquired by clones, nor higher radicality of their amino acid substitutions. Moreover, there was no evidence for fitness degeneration in the old clones compared with that in the younger ones. In summary, although an efficacy of purifying selection may still be reduced in the asexual genomes, our data indicate that its efficiency is not drastically decreased. Even the oldest investigated clone was found to be too young to suffer fitness consequences from a mutation accumulation. This suggests that mechanisms other than mutation accumulation may be needed to explain the competitive advantage of sex in the short term.