共查询到20条相似文献,搜索用时 31 毫秒
1.
Jack Common David Walker‐Sünderhauf Stineke van Houte Edze R. Westra 《Journal of evolutionary biology》2020,33(8):1097-1108
Diversity in host resistance often associates with reduced pathogen spread. This may result from ecological and evolutionary processes, likely with feedback between them. Theory and experiments on bacteria–phage interactions have shown that genetic diversity of the bacterial adaptive immune system can limit phage evolution to overcome resistance. Using the CRISPR–Cas bacterial immune system and lytic phage, we engineered a host–pathogen system where each bacterial host genotype could be infected by only one phage genotype. With this model system, we explored how CRISPR diversity impacts the spread of phage when they can overcome a resistance allele, how immune diversity affects the evolution of the phage to increase its host range and if there was feedback between these processes. We show that increasing CRISPR diversity benefits susceptible bacteria via a dilution effect, which limits the spread of the phage. We suggest that this ecological effect impacts the evolution of novel phage genotypes, which then feeds back into phage population dynamics. 相似文献
2.
Julien Papa?x Jeremy J. Burdon Christian Lannou Peter H. Thrall 《PLoS computational biology》2014,10(5)
Metapopulation processes are important determinants of epidemiological and evolutionary dynamics in host-pathogen systems, and are therefore central to explaining observed patterns of disease or genetic diversity. In particular, the spatial scale of interactions between pathogens and their hosts is of primary importance because migration rates of one species can affect both spatial and temporal heterogeneity of selection on the other. In this study we developed a stochastic and discrete time simulation model to specifically examine the joint effects of host and pathogen dispersal on the evolution of pathogen specialisation in a spatially explicit metapopulation. We consider a plant-pathogen system in which the host metapopulation is composed of two plant genotypes. The pathogen is dispersed by air-borne spores on the host metapopulation. The pathogen population is characterised by a single life-history trait under selection, the infection efficacy. We found that restricted host dispersal can lead to high amount of pathogen diversity and that the extent of pathogen specialisation varied according to the spatial scale of host-pathogen dispersal. We also discuss the role of population asynchrony in determining pathogen evolutionary outcomes. 相似文献
3.
Christopher P. Kozakiewicz Lauren Ricci Austin H. Patton Amanda R. Stahlke Sarah A. Hendricks Mark J. Margres Manuel Ruiz‐Aravena David G. Hamilton Rodrigo Hamede Hamish McCallum Menna E. Jones Paul A. Hohenlohe Andrew Storfer 《Molecular ecology》2020,29(17):3217-3233
Genetic structure in host species is often used to predict disease spread. However, host and pathogen genetic variation may be incongruent. Understanding landscape factors that have either concordant or divergent influence on host and pathogen genetic structure is crucial for wildlife disease management. Devil facial tumour disease (DFTD) was first observed in 1996 and has spread throughout almost the entire Tasmanian devil geographic range, causing dramatic population declines. Whereas DFTD is predominantly spread via biting among adults, devils typically disperse as juveniles, which experience low DFTD prevalence. Thus, we predicted little association between devil and tumour population structure and that environmental factors influencing gene flow differ between devils and tumours. We employed a comparative landscape genetics framework to test the influence of environmental factors on patterns of isolation by resistance (IBR) and isolation by environment (IBE) in devils and DFTD. Although we found evidence for broad‐scale costructuring between devils and tumours, we found no relationship between host and tumour individual genetic distances. Further, the factors driving the spatial distribution of genetic variation differed for each. Devils exhibited a strong IBR pattern driven by major roads, with no evidence of IBE. By contrast, tumours showed little evidence for IBR and a weak IBE pattern with respect to elevation in one of two tumour clusters we identify herein. Our results warrant caution when inferring pathogen spread using host population genetic structure and suggest that reliance on environmental barriers to host connectivity may be ineffective for managing the spread of wildlife diseases. Our findings demonstrate the utility of comparative landscape genetics for identifying differential factors driving host dispersal and pathogen transmission. 相似文献
4.
A. E. Jenns K. J. Leonard 《TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik》1985,69(5-6):503-513
Summary The reliability of analyses of variance for evaluating host cultivar x pathogen isolate specificity in resistance controlled by polygenes with additive effects was tested with combinations of hypothetical host and pathogen genotypes in a model system. In each test, varying numbers of host and pathogen genotypes were combined in all combinations, the resulting disease severities were calculated according to the model, and those data were subjected to analysis of variance. The percentage of total variance accounted for by host x pathogen interaction decreased with increasing numbers of host and pathogen genotypes per test. Simulated selection for virulence among randomly generated pathogen genotypes increased the percentage of variance attributable to host x pathogen genotype interaction, but simulated selection for resistance among host genotypes decreased it. The percentage of variance accounted for by interaction was greatest when selection of resistant host genotypes was followed by selection of the most virulent pathogen genotype on each selected host genotype. When gene frequencies were varied in the model, the interaction variance was greatest at low frequencies of resistance genes and high frequencies of virulence genes, but the number of matches between genes for specific virulence and specific resistance was greatest for high frequencies of both resistance and virulence genes. A simplified method of analysis was developed to estimate the amount of specific resistance in a set of host genotypes inoculated in all combinations with a set of pathogen genotypes. This method, based on the variance of disease severity adjusted to remove general virulence, proved consistently accurate with varying numbers of genotypes in the set, varying numbers of loci for resistance and virulence, and varying frequencies of genes for resistance and virulence. The variance method is of comparable accuracy and is much simpler than the previously proposed methods based on regression analysis. Simulated selection for resistance in the host and for virulence in the pathogen population increased the accuracy of both the variance method and the regression method. 相似文献
5.
Carpenter JA Hadfield JD Bangham J Jiggins FM 《Evolution; international journal of organic evolution》2012,66(4):1114-1125
Genetic correlations between parasite resistance and other traits can act as an evolutionary constraint and prevent a population from evolving increased resistance. For example, previous studies have found negative genetic correlations between host resistance and life-history traits. In invertebrates, the level of resistance often depends on the combination of the host and parasite genotypes, and in this study, we have investigated whether such specific resistance also acts as an evolutionary constraint. We measured the resistance of different genotypes of the fruit fly Drosophila melanogaster to different genotypes of a naturally occurring pathogen, the sigma virus. Using a multitrait analysis, we examine whether genetic covariances alter the potential to select for general resistance against all of the different viral genotypes. We found large amounts of heritable variation in resistance, and evidence for specific interactions between host and parasite, but these interactions resulted in little constraint on Drosophila evolving greater resistance. 相似文献
6.
Amy C. Kelly Nohra E. Mateus-Pinilla William Brown Marilyn O. Ruiz Marlis R. Douglas Michael E. Douglas Paul Shelton Tom Beissel Jan Novakofski 《Population Ecology》2014,56(2):327-340
The landscape can influence host dispersal and density, which in turn, affect infectious disease transmission, spread, and persistence. Understanding how the landscape influences wildlife dispersal and pathogen epidemiology can enhance the efficacy of disease management in natural populations. We applied landscape genetics to examine relationships among landscape variables, dispersal of white-tailed deer hosts and transmission/spread of chronic wasting disease (CWD), a fatal prion encephalopathy. Our focus was on quantifying movements and population structure of host deer in infected areas as a means of predicting the spread of this pathology and promoting its adaptive management. We analyzed microsatellite genotypes of CWD-infected and uninfected deer from two disease foci (Southern Wisconsin, Northern Illinois). We quantified gene flow and population structure using F ST, assignment tests, and spatial autocorrelation analyses. Gene flow estimates were then contrasted against a suite of landscape variables that potentially mediate deer dispersal. Forest fragmentation and grassland connectivity promoted deer movements while rivers, agricultural fields and large urbanized areas impeded movement. Landscape variables, deer dispersal, and disease transmission covaried significantly and positively in our analyses. Habitats with elevated host gene flow supported the concept of dispersal-mediated CWD transmission by reflecting a concomitant, rapid CWD expansion. Large, interrelated social groups isolated by movement barriers overlapped disease foci, suggesting that philopatry exacerbated CWD transmission. Our results promote adaptive management of CWD by predicting patterns of its spread and identifying habitats at risk for invasion. Further, our landscape genetics approach underscores the significance of topography and host behavior in wildlife disease transmission. 相似文献
7.
We investigate the dynamics of a cytoplasmic parasitic element with feminizing effect in a two-population model. We assume that the host species has a ZZ/ZW sex determination system. Our analysis reveals that the feminizer and the W chromosome can stably coexist by dominating different populations if the transmission rate differs significantly between the populations and migration is sufficiently weak. In the equilibrium of coexistence, genetic influx at any host autosomal locus is strongly enhanced in the population where infection is prevalent but not modified in the other population. We further explore conditions for the spread of autosomal suppressor genes that reduce transmission of feminizing elements to the cost of host viability, and compute their equilibrium frequencies. Our results confirm the hypothesis that selfish genetic elements convert infected host populations into genetic sinks, thereby restricting the spread of transmission suppressors. 相似文献
8.
Alice K. E. Ekroth Michael Gerth Emily J. Stevens Suzanne A. Ford Kayla C. King 《The ISME journal》2021,15(7):2146
Pathogens continue to emerge from increased contact with novel host species. Whilst these hosts can represent distinct environments for pathogens, the impacts of host genetic background on how a pathogen evolves post-emergence are unclear. In a novel interaction, we experimentally evolved a pathogen (Staphylococcus aureus) in populations of wild nematodes (Caenorhabditis elegans) to test whether host genotype and genetic diversity affect pathogen evolution. After ten rounds of selection, we found that pathogen virulence evolved to vary across host genotypes, with differences in host metal ion acquisition detected as a possible driver of increased host exploitation. Diverse host populations selected for the highest levels of pathogen virulence, but infectivity was constrained, unlike in host monocultures. We hypothesise that population heterogeneity might pool together individuals that contribute disproportionately to the spread of infection or to enhanced virulence. The genomes of evolved populations were sequenced, and it was revealed that pathogens selected in distantly-related host genotypes diverged more than those in closely-related host genotypes. S. aureus nevertheless maintained a broad host range. Our study provides unique empirical insight into the evolutionary dynamics that could occur in other novel infections of wildlife and humans.Subject terms: Molecular evolution, Bacterial evolution, Bacterial genetics 相似文献
9.
Disease, frequency-dependent selection, and genetic polymorphisms: experiments with stripe rust and wheat 总被引:1,自引:0,他引:1
Abstract.— Pathogens have the potential to maintain genetic polymorphisms by creating frequency-dependent selection on their host. This can occur when a rare host genotype is less likely to be attacked by a pathogen (frequency-dependent disease attack) and has higher fitness at low frequency (negative frequency-dependent selection). In this study, we used wheat genotypes that were susceptible to different races of the pathogen Puccinia striiformis to test whether disease created frequency-selection on its host and whether such selection could maintain polymorphisms for resistance genes in the wheat populations. Four different two-way mixtures of wheat genotypes were planted at different frequencies in both the presence and absence of disease. Disease created frequency-dependent selection on its host in some populations. Unknown factors other than disease also created frequency-dependent selection in this system because, in some instances, rare genotype advantage was observed in the absence of disease. Although the pathogen created frequency-dependent selection on its host, this selection was not sufficient to maintain genetic polymorphism in the host populations. In all cases where frequency-dependent selection occurred only in the diseased plots, one of the two genotypes was predicted to dominate in the population and the same genotype was predicted to dominate in both the presence and absence of disease. Only in cases where frequency-dependent selection was not caused by disease was there evidence that genetic polymorphisms would be maintained in the population. The frequency-dependent selection described in this study is a consequence of epidemiological effects of disease and differs from the time-lagged frequency-dependent selection resulting from coevolution between hosts and parasites. The impact of this direct frequency-dependent selection on the maintenance of genetic polymorphisms in the host population is discussed. 相似文献
10.
Anna-Liisa Laine Jeremy J. Burdon Adnane Nemri Peter H. Thrall 《Proceedings. Biological sciences / The Royal Society》2014,281(1787)
The extent and speed at which pathogens adapt to host resistance varies considerably. This presents a challenge for predicting when—and where—pathogen evolution may occur. While gene flow and spatially heterogeneous environments are recognized to be critical for the evolutionary potential of pathogen populations, we lack an understanding of how the two jointly shape coevolutionary trajectories between hosts and pathogens. The rust pathogen Melampsora lini infects two ecotypes of its host plant Linum marginale that occur in close proximity yet in distinct populations and habitats. In this study, we found that within-population epidemics were different between the two habitats. We then tested for pathogen local adaptation at host population and ecotype level in a reciprocal inoculation study. Even after controlling for the effect of spatial structure on infection outcome, we found strong evidence of pathogen adaptation at the host ecotype level. Moreover, sequence analysis of two pathogen infectivity loci revealed strong genetic differentiation by host ecotype but not by distance. Hence, environmental variation can be a key determinant of pathogen population genetic structure and coevolutionary dynamics and can generate strong asymmetry in infection risks through space. 相似文献
11.
Jason A. Corwin Daniel Copeland Julie Feusier Anushriya Subedy Robert Eshbaugh Christine Palmer Julin Maloof Daniel J. Kliebenstein 《PLoS genetics》2016,12(2)
The most established model of the eukaryotic innate immune system is derived from examples of large effect monogenic quantitative resistance to pathogens. However, many host-pathogen interactions involve many genes of small to medium effect and exhibit quantitative resistance. We used the Arabidopsis-Botrytis pathosystem to explore the quantitative genetic architecture underlying host innate immune system in a population of Arabidopsis thaliana. By infecting a diverse panel of Arabidopsis accessions with four phenotypically and genotypically distinct isolates of the fungal necrotroph B. cinerea, we identified a total of 2,982 genes associated with quantitative resistance using lesion area and 3,354 genes associated with camalexin production as measures of the interaction. Most genes were associated with resistance to a specific Botrytis isolate, which demonstrates the influence of pathogen genetic variation in analyzing host quantitative resistance. While known resistance genes, such as receptor-like kinases (RLKs) and nucleotide-binding site leucine-rich repeat proteins (NLRs), were found to be enriched among associated genes, they only account for a small fraction of the total genes associated with quantitative resistance. Using publically available co-expression data, we condensed the quantitative resistance associated genes into co-expressed gene networks. GO analysis of these networks implicated several biological processes commonly connected to disease resistance, including defense hormone signaling and ROS production, as well as novel processes, such as leaf development. Validation of single gene T-DNA knockouts in a Col-0 background demonstrate a high success rate (60%) when accounting for differences in environmental and Botrytis genetic variation. This study shows that the genetic architecture underlying host innate immune system is extremely complex and is likely able to sense and respond to differential virulence among pathogen genotypes. 相似文献
12.
? Premise of the study: Evolutionary processes that maintain genetic diversity in plants are likely to include selection imposed by pathogens. Negative frequency-dependent selection is a mechanism for maintenance of resistance polymorphism in plant-pathogen interactions. We explored whether such selection operates in the Bromus tectorum-Ustilago bullata pathosystem. Gene-for-gene relationships between resistance and avirulence loci have been demonstrated for this pathosystem. ? Methods: We used molecular markers and cross-inoculation trials to learn whether the SSR genotypes of the host exhibited resistance to co-occurring pathogen races, whether host genotypes within a population had equal disease probability, and whether a common resistance locus and its corresponding avirulence locus exhibited predicted allele frequency changes during an epidemic. ? Key results: Five of six putative resistance loci that conferred resistance to co-occurring pathogen races occurred in common host SSR genotypes. Some common genotypes within populations were more likely to be diseased than others, and genotype frequencies sometimes changed across years in patterns consistent with frequency-dependent selection. Observed changes in frequency of resistance and virulence alleles during an epidemic provided further support, but evidence was inconclusive. ? Conclusions: Frequency-dependent selection may operate at endemic disease levels in this pathosystem, but is difficult to detect because many susceptible plants escape infection. Most pathogen isolates were virulent on most host genotypes, minimizing the apparent importance of frequency-dependent selection even during epidemics. 相似文献
13.
The diversity-disease hypothesis states that decreased genetic diversity in host populations increases the incidence of diseases caused by pathogens (= monoculture effect) and eventually influences ecosystem functioning. The monoculture effect is well-known from crop studies and may be partially specific to the artificial situation in agriculture. The effect received little attention in animal populations of different diversities. Compared with plants, animals are mobile and exhibiting social interactions. We followed the spread of a microsporidian parasite in semi-natural outdoor Daphnia magna populations of low and high genetic diversity. We used randomly selected, naturally occurring host genotypes. Host populations of low diversity were initially monoclonal, while the host populations of high diversity started with 10 genotypes per replicate. We found that the parasite spread significantly better in host populations of low diversity compared with host populations of high diversity, independent of parasite diversity. The difference was visible over a 3-year period. Host genotypic diversity did not affect host population density. Our experiment demonstrated a monoculture effect in independently replicated semi-natural zooplankton populations, indicating that the monoculture effect may be relevant beyond agriculture. 相似文献
14.
15.
Allocation to sexual versus nonsexual disease transmission 总被引:1,自引:0,他引:1
Many diseases have both sexual and nonsexual transmission routes, and closely related diseases often differ in their degree of sexual transmission. We investigate the evolution of transmission mode as a function of host social and mating structure using a model in which disease transmission is explicitly dependent on the numbers of sexual and nonsexual contacts (which are themselves a function of population density) and per-contact infection probabilities. Most generally, and in the absence of trade-offs between the degree of sexual transmission and effects on host fecundity and mortality, nonsexual transmission is favored above the social-sexual crossover point (the host density at which the number of nonsexual contacts exceeds the number of sexual contacts), while sexual transmission is favored below this point. When changes in allocation to the two transmission modes are accompanied by changes in mortality or fecundity, both mixed and pure transmission strategies can be favored. If invading genotypes differ substantially from resident genotypes, genetic polymorphism in transmission mode is possible. The evolutionary outcomes are predictable from a knowledge of the equilibrium population sizes in relation to the social-sexual crossover point. Our results also show that predictions about dynamic outcomes, based on rates of invasion for single pathogens into healthy populations, do not adequately describe the resulting disease prevalence nor predict the subsequent evolutionary dynamics; once invasion of a pathogen has occurred, the conditions for spread of a second pathogen are themselves altered. If the host is considered as a single resource, our results show that two pathogens may coexist on a single resource if they use that resource differentially and have differential feedbacks on resource abundance; such resource feedback effects may be present in other biological systems. 相似文献
16.
Evolution of herbicide resistance in weeds is a growing problem across the world, and it has been suggested that low herbicide rates may be contributing to this problem. An individual-based simulation model that represents weed population dynamics and the evolution of polygenic herbicide resistance was constructed and used to investigate whether using lower herbicide rates or standard rates at reduced efficacy could reduce the sustainability of cropping systems by causing faster increases in weed population density as herbicide resistance develops. A number of different possible genetic bases for resistance were considered, including monogenic resistance and polygenic resistance conferred by several genes. The results show that cutting herbicide rates does not affect the rate at which weed densities reach critical levels when resistance is conferred exclusively by a single dominant gene. In some polygenic situations, cutting herbicide rates substantially reduces sustainability, due to a combination of faster increase in resistance gene frequency and reduced kill rates in all genotypes, while in other polygenic situations the effect is small. Differences in sustainability depend on combined strength of the resistance genes, variability in phenotypic susceptibility and rate delivered, level of control due to alternative measures, and degree of genetic dominance and epistasis. In the situation where resistance can be conferred by both a single dominant major gene or a number of co-dominant minor genes in combination, the difference made by low rates depends on the relative initial frequency of the major and minor genes. These results show that careful consideration of herbicide rate and understanding the genetic basis of resistance are important aspects of weed management. 相似文献
17.
Helen M. Alexander Robert D. Holt 《Perspectives in Plant Ecology, Evolution and Systematics》1998,1(2):206-220
It is well documented that pathogens can affect the survival, reproduction, and growth of individual plants. Drawing together insights from diverse studies in ecology and agriculture, we evaluate the evidence for pathogens affecting competitive interactions between plants of both the same and different species. Our objective is to explore the potential ecological and evolutionary consequences of such interactions. First, we address how disease interacts with intraspecific competition and present a simple graphical model suggesting that diverse outcomes should be expected. We conclude that the presence of pathogens may have either large or minimal effects on population dynamics depending on many factors including the density-dependent compensatory ability of healthy plants and spatial patterns of infection. Second, we consider how disease can alter competitive abilities of genotypes, and thus may affect the genetic composition of populations. These genetic processes feed back on population dynamics given trade-offs between disease resistance and other fitness components. Third, we examine how the effect of disease on interspecific plant interactions may have potentially far-reaching effects on community composition. A host-specific pathogen, for example, may alter a competitive hierarchy that exists between host and non-host species. Generalist pathogens can also induce indirect competitive interactions between host species. We conclude by highlighting lacunae in our current understanding and suggest that future studies should (1) examine a broader taxonomic range of pathogens since work to date has largely focused on fungal pathogens; (2) increase the use of field competition studies; (3) follow interactions for multiple generations; (4) characterize density-dependent processes; and (5) quantify pathogen, as well as plant, population and community dynamics. 相似文献
18.
Hamilton R Boots M Paterson S 《Proceedings. Biological sciences / The Royal Society》2005,272(1573):1647-1653
Understanding the processes that shape the genetic structure of parasite populations and the functional consequences of different parasite genotypes is critical for our ability to predict how an infection can spread through a host population and for the design of effective vaccines to combat infection and disease. Here, we examine how the genetic structure of parasite populations responds to host genetic heterogeneity. We consider the well-characterized molecular specificity of major histocompatibility complex binding of antigenic peptides to derive deterministic and stochastic models. We use these models to ask, firstly, what conditions favour the evolution of generalist parasite genotypes versus specialist parasite genotypes? Secondly, can parasite genotypes coexist in a population? We find that intragenomic interactions between parasite loci encoding antigenic peptides are pivotal in determining the outcome of evolution. Where parasite loci interact synergistically (i.e. the recognition of additional antigenic peptides has a disproportionately large effect on parasite fitness), generalist parasite genotypes are favoured. Where parasite loci act multiplicatively (have independent effects on fitness) or antagonistically (have diminishing effects on parasite fitness), specialist parasite genotypes are favoured. A key finding is that polymorphism is not stable and that, with respect to functionally important antigenic peptides, parasite populations are dominated by a single genotype. 相似文献
19.
Abstract Virulence is thought to be a driving force in host–pathogen coevolution. Theoretical models suggest that virulence is an unavoidable consequence of pathogens evolving towards a high rate of intrahost reproduction. These models predict a positive correlation between the reproductive fitness of a pathogen and its level of virulence. Theoretical models also suggest that the demography and genetic structure of a host population can influence the evolution of virulence. If evolution occurs faster in pathogen populations than in host populations, the predicted result is local adaptation of the pathogen population. In our studies, we used a combination of molecular and physiological markers to test these hypotheses in an agricultural system. We isolated five strains of the fungal pathogen Mycosphaerella graminicola from each of two wheat cultivars that differed in their level of resistance to this pathogen. Each of the 10 fungal strains had distinct genotypes as indicated by different DNA fingerprints. These fungal strains were re‐inoculated onto the same two host cultivars in a field experiment and their genotype frequencies were monitored over several generations of asexual reproduction. We also measured the virulence of these 10 fungal strains and correlated it to the reproductive fitness of each fungal strain. We found that host genotypes had a strong impact on the dynamics of the pathogen populations. The pathogen population collected from the moderately resistant cultivar Madsen showed greater stability, higher genotype diversity, and smaller selection coefficients than the pathogen populations collected from the susceptible cultivar Stephens or a mixture of the two host cultivars. The pathogen collection from the mixed host population was midway between the two pure lines for most parameters measured. Our results also revealed that the measures of reproductive fitness and virulence of a pathogen strain were not always correlated. The pathogen strains varied in their patterns of local adaptation, ranging from locally adapted to locally maladapted. 相似文献
20.
Pathogens are a main driving force of the evolution of plants and animals. Being resistant to diseases confers a high selective advantage to hosts, yet many host–pathogen systems show a remarkable degree of polymorphism of host resistance and pathogen virulence. The most common explanation of this phenomenon is that both resistance and virulence genes are costly and that there is selection against those genes when they are unnecessary. Here, we use stochastic multi‐locus simulations to show that the origin and the maintenance of genetic polymorphism in plant–pathogen systems can be explained without costs. In multi‐locus gene‐for‐gene systems, temporal domination of a super pathogen can cause polymorphism in resistance through neutral drift. With an increasing number of susceptible alleles in the host population, pathogen types other than the super race are able to cause infections and invade the population, leading to higher pathogen diversity and in turn to higher host diversity. 相似文献