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1.
Hosts are armed with several lines of defence in the battle against parasites: they may prevent the establishment of infection, reduce parasite growth once infected or persevere through mechanisms that reduce the damage caused by infection, called tolerance. Studies on tolerance in animals have focused on mortality, and sterility tolerance has not been investigated experimentally. Here, we tested for genetic variation in the multiple steps of defence when the invertebrate Daphnia magna is infected with the sterilizing bacterial pathogen Pasteuria ramosa: anti-infection resistance, anti-growth resistance and the ability to tolerate sterilization once infected. When exposed to nine doses of a genetically diverse pathogen inoculum, six host genotypes varied in their average susceptibility to infection and in their parasite loads once infected. How host fecundity changed with increasing parasite loads did not vary between genotypes, indicating that there was no genetic variation for this measure of fecundity tolerance. However, genotypes differed in their level of fecundity compensation under infection, and we discuss how, by increasing host fitness without targeting parasite densities, fecundity compensation is consistent with the functional definition of tolerance. Such infection-induced life-history shifts are not traditionally considered to be part of the immune response, but may crucially reduce harm (in terms of fitness loss) caused by disease, and are a distinct source of selection on pathogens. 相似文献
2.
An artificial selection experiment designed to explore the evolution of resistance to a fungal pathogen, Beauveria bassiana, in Drosophila melanogaster is reported here. The experiment was designed to test whether there is sufficient additive genetic variation in this trait for increased resistance to evolve, and, if so, whether there are correlated responses that might represent a cost to defence. After 15 generations of selection, flies from selected lines did not have higher overall fitness after infection compared with control lines. The response to selection for resistance against this pathogen is thus much weaker than against other species, in particular, parasitoids. There was, however, evidence for increased late-life fecundity in selected lines, which may indicate evolved tolerance of fungal infection. This increase was accompanied by reduced early-life fitness, which may reflect the well-known trade-off between early and late reproduction. In the absence of fungal infection, selected flies had lower fitness than control flies, and the possibility that this is also a trade-off with increased tolerance is explored. 相似文献
3.
Benjamin J. Parker Justine R. Garcia Nicole M. Gerardo 《Evolution; international journal of organic evolution》2014,68(8):2421-2429
Individuals vary in their ability to defend against pathogens. Determining how natural selection maintains this variation is often difficult, in part because there are multiple ways that organisms defend themselves against pathogens. One important distinction is between mechanisms of resistance that fight off infection, and mechanisms of tolerance that limit the impact of infection on host fitness without influencing pathogen growth. Theory predicts variation among genotypes in resistance, but not necessarily in tolerance. Here, we study variation among pea aphid (Acyrthosiphon pisum) genotypes in defense against the fungal pathogen Pandora neoaphidis. It has been well established that pea aphids can harbor symbiotic bacteria that protect them from fungal pathogens. However, it is unclear whether aphid genotypes vary in defense against Pandora in the absence of protective symbionts. We therefore measured resistance and tolerance to fungal infection in aphid lines collected without symbionts, and found variation among lines in survival and in the percent of individuals that formed a sporulating cadaver. We also found evidence of variation in tolerance to the effects of pathogen infection on host fecundity, but no variation in tolerance of pathogen‐induced mortality. We discuss these findings in light of theoretical predictions about host‐pathogen coevolution. 相似文献
4.
5.
Insects are exposed to a variety of potential pathogens in their environment, many of which can severely impact fitness and health. Consequently, hosts have evolved resistance and tolerance strategies to suppress or cope with infections. Hosts utilizing resistance improve fitness by clearing or reducing pathogen loads, and hosts utilizing tolerance reduce harmful fitness effects per pathogen load. To understand variation in, and selective pressures on, resistance and tolerance, we asked to what degree they are shaped by host genetic background, whether plasticity in these responses depends upon dietary environment, and whether there are interactions between these two factors. Females from ten wild‐type Drosophila melanogaster genotypes were kept on high‐ or low‐protein (yeast) diets and infected with one of two opportunistic bacterial pathogens, Lactococcus lactis or Pseudomonas entomophila. We measured host resistance as the inverse of bacterial load in the early infection phase. The relationship (slope) between fly fecundity and individual‐level bacteria load provided our fecundity tolerance measure. Genotype and dietary yeast determined host fecundity and strongly affected survival after infection with pathogenic P. entomophila. There was considerable genetic variation in host resistance, a commonly found phenomenon resulting from for example varying resistance costs or frequency‐dependent selection. Despite this variation and the reproductive cost of higher P. entomophila loads, fecundity tolerance did not vary across genotypes. The absence of genetic variation in tolerance may suggest that at this early infection stage, fecundity tolerance is fixed or that any evolved tolerance mechanisms are not expressed under these infection conditions. 相似文献
6.
Hurd H Taylor PJ Adams D Underhill A Eggleston P 《Evolution; international journal of organic evolution》2005,59(12):2560-2572
Costly resistance mechanisms have been cited as an explanation for the widespread occurrence of parasitic infections, yet few studies have examined these costs in detail. A malaria-mosquito model has been used to test this concept by making a comparison of the fitness of highly susceptible lines of mosquitoes with lines that are resistant to infection. Malaria infection is known to cause a decrease in fecundity and fertility of mosquitoes; resistant mosquitoes were thus predicted to be fitter than susceptible ones. Anopheles gambiae were selected for refractoriness/resistance or for increased susceptibility to infection by Plasmodium yoelii nigeriensis. Additional lines that acted as controls for inbreeding depression were raised in parallel but not exposed to selection pressure. Selections were made in triplicate so that founder effects could be detected. Resistance mechanisms that were selected included melanotic encapsulation of parasites within 24 h postinfection and the complete disappearance of parasites from the gut. Costs of immune surveillance were assessed after an uninfected feed, and costs of immune deployment were assessed after exposure to infection and to infection and additional stresses. Mosquito survivorship was unaffected by either resistance to infection or by an increased burden of infection when compared with low levels of infection. In most cases reproductive fitness was equally affected by refractoriness or by infection. Resistant mosquitoes did not gain a fitness advantage by eliminating the parasites. Costs were consistently associated with larval production and egg hatch rate but rarely attributed to changes in blood feeding and never to changes in mosquito size. No advantages appeared to be gained by the offspring of resistant mosquitoes. Furthermore, we were unable to select for refractoriness in groups of mosquitoes in which 100% or 50% of the population were exposed to infection every generation for 22 generations. Under these selection pressures, no population had become completely refractory and only one became more resistant. Variations in fitness relative to control lines in different groups were attributed to founder effects. Our conclusion from these findings is that refractoriness to malaria is as costly as tolerance of infection. 相似文献
7.
Marcus J. O. Watson Ary A. Hoffmann 《Evolution; international journal of organic evolution》1996,50(3):1182-1192
The way populations respond to selection can be altered when populations are acclimated prior to selection. To examine this possibility, the responses of replicate lines of Drosophila melanogaster and D. simulans to selection for increased resistance to cold were compared. Flies were selected without hardening or after they had been hardened by holding them at 4°C for one hour. The selection response in both species was much greater when flies were not cold-hardened. Cold resistance in both sets of selected lines reached a plateau after a few generations. Surprisingly, continued selection for increased resistance resulted in decreasing levels of resistance. This decrease was no longer evident after selection had been relaxed for a generation, suggesting cross-generation effects. The magnitude of the cross-generation effects increased with additional generations of selection. Cross-generation effects were also detected for fitness components. Relaxing selection for a generation increased fecundity, weight, viability, and development time. Comparisons of relaxed lines and control lines indicated that only fecundity was influenced by selection. Both sets of selected lines had a lower fecundity than control lines. Crosses between control and selected lines and among replicate selected lines indicated that this decrease in fecundity was not associated with inbreeding. The direct and correlated responses to selection for cold resistance can therefore be influenced by acclimation and cross-generation effects. 相似文献
8.
Pathogens and parasites can be strong agents of selection, and often exhibit some degree of genetic specificity for individual
host strains. Here we show that this host–pathogen specificity can affect the evolution of host life history traits. All else
equal, evolution should select for genes that increase individuals' reproduction rates or lifespans (and thus total reproduction
per individual). Using a simple host–pathogen model, we show that when the genetic specificity of pathogen infection is low,
host strains with higher reproduction rates or longer lifespans drive slower-reproducing or shorter-lived host strains to
extinction, as one would expect. However, when pathogens exhibit specificity for host strains with different life history
traits, the evolutionary advantages of these traits can be greatly diminished by pathogen-mediated selection. Given sufficient
host–pathogen specificity, pathogen-mediated selection can maintain polymorphism in host traits that are correlated with pathogen
resistance traits, despite large intrinsic fitness differences among host strains. These results have two important implications.
First, selection on host life history traits will be weaker than expected, whenever host fitness is significantly affected
by genotype-specific pathogen attack. Second, where polymorphism in host traits is maintained by pathogen-mediated selection,
preserving the genetic diversity of host species may require preserving their pathogens as well.
This revised version was published online in November 2006 with corrections to the Cover Date. 相似文献
9.
Carolin C. Wendling K. Mathias Wegner 《Proceedings. Biological sciences / The Royal Society》2015,282(1804)
One hypothesis for the success of invasive species is reduced pathogen burden, resulting from a release from infections or high immunological fitness of invaders. Despite strong selection exerted on the host, the evolutionary response of invaders to newly acquired pathogens has rarely been considered. The two independent and genetically distinct invasions of the Pacific oyster Crassostrea gigas into the North Sea represent an ideal model system to study fast evolutionary responses of invasive populations. By exposing both invasion sources to ubiquitous and phylogenetically diverse pathogens (Vibrio spp.), we demonstrate that within a few generations hosts adapted to newly encountered pathogen communities. However, local adaptation only became apparent in selective environments, i.e. at elevated temperatures reflecting patterns of disease outbreaks in natural populations. Resistance against sympatric and allopatric Vibrio spp. strains was dominantly inherited in crosses between both invasion sources, resulting in an overall higher resistance of admixed individuals than pure lines. Therefore, we suggest that a simple genetic resistance mechanism of the host is matched to a common virulence mechanism shared by local Vibrio strains. This combination might have facilitated a fast evolutionary response that can explain another dimension of why invasive species can be so successful in newly invaded ranges. 相似文献
10.
Janis Antonovics Mike Boots Dieter Ebert Britt Koskella Mary Poss Ben M. Sadd 《Evolution; international journal of organic evolution》2013,67(1):1-9
Most species seem to be completely resistant to most pathogens and parasites. This resistance has been called “nonhost resistance” because it is exhibited by species that are considered not to be part of the normal host range of the pathogen. A conceptual model is presented suggesting that failure of infection on nonhosts may be an incidental by‐product of pathogen evolution leading to specialization on their source hosts. This model is contrasted with resistance that results from hosts evolving to resist challenge by their pathogens, either as a result of coevolution with a persistent pathogen or as the result of one‐sided evolution by the host against pathogens that are not self‐sustaining on those hosts. Distinguishing evolved from nonevolved resistance leads to contrasting predictions regarding the relationship between resistance and genetic distance. An analysis of cross‐inoculation experiments suggests that the resistance is often the product of pathogen specialization. Understanding the contrasting evolutionary origins of resistance is critical for studies on the genetics and evolution of host–pathogen interactions in human, agricultural, and natural populations. Research on human infectious disease using animal models may often study resistances that have quite contrasting evolutionary origins, and therefore very different underlying genetic mechanisms. 相似文献
11.
Background
When organisms are attacked by multiple natural enemies, the evolution of a resistance mechanism to one natural enemy will be influenced by the degree of cross-resistance to another natural enemy. Cross-resistance can be positive, when a resistance mechanism against one natural enemy also offers resistance to another; or negative, in the form of a trade-off, when an increase in resistance against one natural enemy results in a decrease in resistance against another. Using Drosophila melanogaster, an important model system for the evolution of invertebrate immunity, we test for the existence of cross-resistance against parasites and pathogens, at both a phenotypic and evolutionary level.Methods
We used a field strain of D. melanogaster to test whether surviving parasitism by the parasitoid Asobara tabida has an effect on the resistance against Beauveria bassiana, an entomopathogenic fungus; and whether infection with the microsporidian Tubulinosema kingi has an effect on the resistance against A. tabida. We used lines selected for increased resistance to A. tabida to test whether increased parasitoid resistance has an effect on resistance against B. bassiana and T. kingi. We used lines selected for increased tolerance against B. bassiana to test whether increased fungal resistance has an effect on resistance against A. tabida.Results/Conclusions
We found no positive cross-resistance or trade-offs in the resistance to parasites and pathogens. This is an important finding, given the use of D. melanogaster as a model system for the evolution of invertebrate immunity. The lack of any cross-resistance to parasites and pathogens, at both the phenotypic and the evolutionary level, suggests that evolution of resistance against one class of natural enemies is largely independent of evolution of resistance against the other. 相似文献12.
Juvenile hormone as a regulator of the trade-off between reproduction and life span in Drosophila melanogaster 总被引:2,自引:0,他引:2
Trade-offs between reproduction and life span are ubiquitous, but little is known about their underlying mechanisms. Here we combine treatment with the juvenile hormone analog (JHa) methoprene and experimental evolution in Drosophila melanogaster to study the potential role of juvenile hormone (JH) in mediating such trade-offs at both the physiological and evolutionary level. Exposure to JHa in the larval medium (and up to 24 h posteclosion) increased early life fecundity but reduced life span of normal (unselected) flies, supporting the physiological role of JH in mediating the trade-off. This effect was much smaller for life span, and not detectable for fecundity, in fly lines previously bred for 19 generations on a medium containing JHa. Furthermore, these selection lines lived longer than unselected controls even in the absence of JHa treatment, without a detectable reduction in early life fecundity. Thus, selection for resistance to JHa apparently induced some evolutionary changes in JH metabolism or signaling, which led to longer life span as a correlated response. This supports the hypothesis that JH may mediate evolution of longer life span, but--contrary to our expectation-this apparently does not need to trade--off with fecundity. 相似文献
13.
Concurrent evolution of resistance and tolerance to pathogens 总被引:1,自引:0,他引:1
Recent experiments on plant defenses against pathogens or herbivores have shown various patterns of the association between resistance, which reduces the probability of being infected or attacked, and tolerance, which reduces the loss of fitness caused by the infection or attack. Our study describes the simultaneous evolution of these two strategies of defense in a population of hosts submitted to a pathogen. We extended previous approaches by assuming that the two traits are independent (e.g., determined by two unlinked genes), by modeling different shapes of the costs of defenses, and by taking into account the demographic and epidemiological dynamics of the system. We provide novel predictions on the variability and the evolution of defenses. First, resistance and tolerance do not necessarily exclude each other; second, they should respond in different ways to changes in parameters that affect the epidemiology or the relative costs and benefits of defenses; and third, when comparing investments in defenses among different environments, the apparent associations among resistance, tolerance, and fecundity in the absence of parasites can lead to the false conclusion that only one defense trait is costly. The latter result emphasizes the problems of estimating trade-offs and costs among natural populations without knowledge of the underlying mechanisms. 相似文献
14.
Tadeusz J. Kawecki 《Evolution; international journal of organic evolution》2020,74(2):338-348
Mechanisms of resistance to pathogens and parasites are thought to be costly and thus to lead to evolutionary trade-offs between resistance and life-history traits expressed in the absence of the infective agents. On the other hand, sexually selected traits are often proposed to indicate “good genes” for resistance, which implies a positive genetic correlation between resistance and success in sexual selection. Here I show that experimental evolution of improved resistance to the intestinal pathogen Pseudomonas entomophila in Drosophila melanogaster was associated with a reduction in male sexual success. Males from four resistant populations achieved lower paternity than males from four susceptible control populations in competition with males from a competitor strain, indicating an evolutionary cost of resistance in terms of mating success and/or sperm competition. In contrast, no costs were found in larval viability, larval competitive ability and population productivity assayed under nutritional limitation; together with earlier studies this suggests that the costs of P. entomophila resistance for nonsexual fitness components are negligible. Thus, rather than indicating heritable pathogen resistance, sexually selected traits expressed in the absence of pathogens may be sensitive to costs of resistance, even if no such costs are detected in other fitness traits. 相似文献
15.
Anderson JB 《Nature reviews. Microbiology》2005,3(7):547-556
Like other microorganisms, fungi exist in populations that are adaptable. Under the selection imposed by antifungal drugs, drug-sensitive fungal pathogens frequently evolve resistance. Although the molecular mechanisms of resistance are well-characterized, there are few measurements of the impact of these mechanisms on pathogen fitness in different environments. To predict resistance before a new drug is prescribed in the clinic, the full spectrum of potential resistance mutations and the interactions among combinations of divergent mechanisms can be determined in evolution experiments. In the search for new strategies to manage drug resistance, measuring the limits of adaptation might reveal methods for trapping fungal pathogens in evolutionary dead ends. 相似文献
16.
Abstract. 1. Defence against parasites and pathogens can be essential, yet not all hosts respond similarly to parasitic challenge. Environmental conditions are thought to explain variation in host responses to parasites.
2. Lestes forcipatus damselflies emerging later in the season have shown higher resistance to the mite, Arrenurus planus , than hosts emerging earlier. This study was undertaken to determine whether variation in environmental temperatures characteristic of early vs. late emergence times, degree or costs of mite parasitism, and/or size of newly emerged adults could explain seasonal variation in defence and resistance to ectoparasitic mites.
3. In this study damselflies from early vs. late emergence groups differed in size at emergence and mite intensity. In general, early hosts were larger and had more mites than later hosts. However only experimental temperatures experienced by damselflies at emergence influenced defence and resistance against mites and not host size or degree of parasitism.
4. More specifically, hosts from early and late emergence groups did not differ in defence and resistance when held at the same temperatures in incubators. Housing at a high temperature, indicative of later in the season, was associated with higher defence and resistance for damselflies from both early and late emergence groups.
5. These results indicate that daily temperatures in relation to emergence timing can account for seasonal increases in resistance for this temperate insect. Seasonal increases in resistance may be expected for other temperate insect–parasite associations and should have important implications for the phenology of parasites and for seasonal variation in parasite-mediated selection. 相似文献
2. Lestes forcipatus damselflies emerging later in the season have shown higher resistance to the mite, Arrenurus planus , than hosts emerging earlier. This study was undertaken to determine whether variation in environmental temperatures characteristic of early vs. late emergence times, degree or costs of mite parasitism, and/or size of newly emerged adults could explain seasonal variation in defence and resistance to ectoparasitic mites.
3. In this study damselflies from early vs. late emergence groups differed in size at emergence and mite intensity. In general, early hosts were larger and had more mites than later hosts. However only experimental temperatures experienced by damselflies at emergence influenced defence and resistance against mites and not host size or degree of parasitism.
4. More specifically, hosts from early and late emergence groups did not differ in defence and resistance when held at the same temperatures in incubators. Housing at a high temperature, indicative of later in the season, was associated with higher defence and resistance for damselflies from both early and late emergence groups.
5. These results indicate that daily temperatures in relation to emergence timing can account for seasonal increases in resistance for this temperate insect. Seasonal increases in resistance may be expected for other temperate insect–parasite associations and should have important implications for the phenology of parasites and for seasonal variation in parasite-mediated selection. 相似文献
17.
ALEJANDRA C. SCANNAPIECO PABLO SAMBUCETTI FABIAN M. NORRY 《Biological journal of the Linnean Society. Linnean Society of London》2009,97(4):738-748
The possible associations between longevity, early fecundity, and stress-resistance traits were explored using artificial selection on longevity in a laboratory population of Drosophila buzzatii . Three replicated lines were selected for increased lifespan (L lines) and compared with the respective unselected controls (C lines) after the 14th generation of selection. Mean longevity exhibited a significant response to selection. The baseline mortality tended to decrease in the L lines and a negative correlated response to longevity selection was found for early fecundity. Egg-to-adult developmental time increased in L lines. Longevity selection increased stress resistance for both high and low temperatures, as measured by heat knockdown resistance and chill-coma recovery. Starvation resistance also tended to be higher in L than in C lines. The results obtained are consistent with the hypothesis of trade-offs between longevity and early fecundity, and also suggest a trade-off association between adult longevity and developmental time. Correlated selection responses were generally consistent with correlations among the traits previously inferred from altitudinal clines for longevity and stress-resistance phenotypes. © 2009 The Linnean Society of London, Biological Journal of the Linnean Society , 2009, 97 , 738–748. 相似文献
18.
Aims Many resistance genes against fungal pathogens show costs of resistance. Genetically modified (GM) plants that differ in only one or a few resistance genes from control plants present ideal systems for measuring these costs in the absence of pathogens.Methods To assess the ecological relevance of costs of pathogen resistance, we grew individual plants of four transgenic spring wheat lines in a field trial with three pathogen levels and varied the genetic diversity of the crop.Important findings We found that two lines with a Pm3b transgene were more resistant to powdery mildew than their sister lines of the variety Bobwhite, whereas lines with chitinase (A9) or chitinase and glucanase (A13) transgenes were not more resistant than their mother variety Frisal. Nevertheless, in the absence of the pathogen, both the GM lines of Bobwhite as well as those of Frisal performed significantly worse than their controls, i.e. Pm3b #1 and Pm3b #2 had 39% or 53% and A9 and A13 had 14% or 23% lower yields. In the presence of the pathogen, all GM lines except Pm3b #2 could increase their yields and other fitness-related traits, reaching the performance levels of the control lines. Line Pm3b #2 seemed to have lost its phenotypic plasticity and had low performance in all environments. This may have been caused by very high transgene expression. No synergistic effects of mixing different GM lines with each other were detected. This might have been due to high transgene expression or the similarity between the lines regarding their resistance genes. We conclude that costs of resistance can be high for transgenic plants with constitutive transgene expression and that this can occur even in cases where the non-transgenic control lines are already relatively resistant, such as in our variety Frisal. Transgenic plants could only compete with conventional varieties in environments with high pathogen pressure. Furthermore, the large variability among the GM lines, which may be due to unpredictable transgene expression, suggests that case-by-case assessments are necessary to evaluate costs of resistance. 相似文献
19.
Breakdown in correlations during laboratory evolution. I. Comparative analyses of Drosophila populations 总被引:2,自引:0,他引:2
Phelan JP Archer MA Beckman KA Chippindale AK Nusbaum TJ Rose MR 《Evolution; international journal of organic evolution》2003,57(3):527-535
We provide evidence from comparisons of populations of Drosophila that evolutionary correlations between longevity and stress resistance break down over the course of laboratory evolution. Using 15 distinct evolutionary regimes, we created 75 populations that were differentiated for early fecundity, longevity, starvation resistance, desiccation resistance, and developmental time. In earlier experiments, selection for postponed aging produced increases in stress resistance, whereas selection for increased stress resistance produced increases in longevity. Direct estimates of correlations also indicated an antagonistic relationship between early fecundity on one hand and longevity or stress resistance on the other. Laboratory evolution of extreme values of stress resistance, however, led to a breakdown in these evolutionary relationships. There was no evidence that these significant changes in correlation resulted from genotype-by-environment interactions or inbreeding. These findings suggest that correlations between functional characters are not necessarily durable features of a species, and that short-term evolutionary responses cannot be extrapolated reliably to longer-term evolutionary patterns. 相似文献
20.
Alex Best y White Mike Boots 《Evolution; international journal of organic evolution》2010,64(2):348-357
The disease caused by parasites and pathogens often causes sublethal effects that reduce host fecundity. Theory suggests that if parasites can "target" the detrimental effects of their growth on either host mortality or fecundity, they should always fully sterilize. This is because a reduction in host fecundity does not reduce the infectious period and is therefore neutral to a horizontally transmitted infectious organism. However, in nature fully castrating parasites are relatively rare, no doubt in part because of defense mechanisms in the host. Here, we examine in detail the evolution of host defense to the sterilizing effects of parasites and show that intermediate levels of sterility tolerance are found to evolve for a wide range of cost structures. Our key result arises when the host and parasite coevolve. Investment in tolerance by the host may prevent castration, but if host defense is through resistance (by controlling the parasite's growth rate) coevolution by the parasite results in the complete loss of infected host fecundity. Resistance is therefore a waste of resources, but tolerance can explain why parasites do not castrate their hosts. Our results further emphasize the importance of tolerance as opposed to resistance to parasites. 相似文献