scholarly journals Parasitoid wasps influence where aphids die via an interspecific indirect genetic effect

2013 ◽  
Vol 9 (3) ◽  
pp. 20121151 ◽  
Author(s):  
Mouhammad Shadi Khudr ◽  
Johan A. Oldekop ◽  
David M. Shuker ◽  
Richard F. Preziosi

Host–parasite interactions are a key paradigm for understanding the process of coevolution. Central to coevolution is how genetic variation in interacting species allows parasites to evolve manipulative strategies. However, genetic variation in the parasite may also be associated with host phenotype changes, thereby changing the selection on both species. For instance, parasites often induce changes in the behaviour of their host to maximize their own fitness, yet the quantitative genetic basis for behavioural manipulation has not been fully demonstrated. Here, we show that the genotype of the parasitoid wasp Aphidius ervi has a significant effect on where its aphid host Acyrthosiphon pisum moves to die following parasitism, including the likelihood that the aphid abandons the plant. These results provide a clear example of an interspecific indirect genetic effect whereby the genetics of one species influences the expression of a specific behavioural trait in another.

2021 ◽  
Author(s):  
Samuel Alexander Purkiss ◽  
Mouhammad Shadi Khudr ◽  
Oscar Enrique Aguinaga ◽  
Reinmar Hager

Host-parasite interactions represent complex co-evolving systems in which genetic variation within a species can significantly affect selective pressure on traits in the other (for example via inter-species indirect genetic effects). While often viewed as a two-species interaction between host and parasite species, some systems are more complex due to the involvement of symbionts in the host that influence its immunity, enemies of the host, and the parasite through intraguild predation. However, it remains unclear what the joint effects of intraguild predation, defensive endosymbiosis, within-species genetic variation and indirect genetic effects on host immunity are. We have addressed this question in an important agricultural pest system, the pea aphid Acyrthosiphon pisum, which shows significant intraspecific variability in immunity to the parasitoid wasp Aphidius ervi due to immunity conferring endosymbiotic bacteria. In a complex experiment involving a quantitative genetic design of the parasitoid, two ecologically different aphid lineages and the aphid lion Chrysoperla carnea as an intraguild predator, we demonstrate that aphid immunity is affected by intraspecific genetic variation in the parasitoid and the aphid, as well as by associated differences in the defensive endosymbiont communities. Using 16s rRNA sequencing, we identified secondary symbionts that differed between the lineages. We further show that aphid lineages differ in their altruistic behaviour once parasitised whereby infested aphids move away from the clonal colony to facilitate predation. The outcome of these complex between-species interactions not only shape important host-parasite systems but have also implications for understanding the evolution of multitrophic interactions, and aphid biocontrol.


BMC Genomics ◽  
2014 ◽  
Vol 15 (1) ◽  
pp. 342 ◽  
Author(s):  
Dominique Colinet ◽  
Caroline Anselme ◽  
Emeline Deleury ◽  
Donato Mancini ◽  
Julie Poulain ◽  
...  

PLoS ONE ◽  
2020 ◽  
Vol 15 (11) ◽  
pp. e0242159
Author(s):  
Ailsa H. C. McLean ◽  
Benjamin J. Parker

Evolutionary interactions between parasitoid wasps and insect hosts have been well studied at the organismal level, but little is known about the molecular mechanisms that insects use to resist wasp parasitism. Here we study the interaction between a braconid wasp (Aphidius ervi) and its pea aphid host (Acyrthosiphon pisum). We first identify variation in resistance to wasp parasitism that can be attributed to aphid genotype. We then use transcriptome sequencing to identify genes in the aphid genome that are differentially expressed at an early stage of parasitism, and we compare these patterns in highly resistant and susceptible aphid host lines. We find that resistant genotypes are upregulating genes involved in carbohydrate metabolism and several key innate immune system genes in response to parasitism, but that this response seems to be weaker in susceptible aphid genotypes. Together, our results provide a first look into the complex molecular mechanisms that underlie aphid resistance to wasp parasitism and contribute to a broader understanding of how resistance mechanisms evolve in natural populations.


PeerJ ◽  
2017 ◽  
Vol 5 ◽  
pp. e3559 ◽  
Author(s):  
Cinthya M. Villegas ◽  
Vladimir Žikić ◽  
Saša S. Stanković ◽  
Sebastián A. Ortiz-Martínez ◽  
Ainara Peñalver-Cruz ◽  
...  

BackgroundParasitoids are frequently used in biological control due to the fact that they are considered host specific and highly efficient at attacking their hosts. As they spend a significant part of their life cycle within their hosts, feeding habits and life history of their host can promote specialization via host-race formation (sequential radiation). The specialized host races from different hosts can vary morphologically, behaviorally and genetically. However, these variations are sometimes inconspicuous and require more powerful tools in order to detect variation such as geometric morphometrics analysis.MethodsWe examinedAphidius ervi, an important introduced biological control agent in Chile associated with a great number of aphid species, which are exploiting different plant hosts and habitats. Several combinations (biotypes) of parasitoids with various aphid/host plant combinations were analyzed in order to obtain measures of forewing shape and size. To show the differences among defined biotypes, we chose 13 specific landmarks on each individual parasitoid wing. The analysis of allometric variation calculated in wing shape and size over centroid size (CS), revealed the allometric changes among biotypes collected from different hosts. To show all differences in shape of forewings, we made seven biotype pairs using an outline-based geometric morphometrics comparison.ResultsThe biotypeA. pis_pea(Acyrthosiphon pisumon pea) was the extreme wing size in this study compared to the other analyzed biotypes. Aphid hosts have a significant influence in the morphological differentiation of the parasitoid forewing, splitting biotypes in two groups. The first group consisted of biotypes connected withAcyrthosiphon pisumon legumes, while the second group is composed of biotypes connected with aphids attacking cereals, with the exception of theR. pad_wheat(Rhopalosiphum padion wheat) biotype. There was no significant effect of plant species on parasitoid wing size and shape.DiscussionAlthough previous studies have suggested that the genotype of parasitoids is of greater significance for the morphological variations of size and shape of wings, this study indicates that the aphid host on whichA. ervidevelops is the main factor to alter the structure of parasitoid forewings. Bigger aphid hosts implied longer and broader forewings ofA. ervi.


2021 ◽  
Author(s):  
Melanie R. Smee ◽  
Sally A. Raines ◽  
Julia Ferrari

AbstractMicrobial symbionts often alter the phenotype of their host. Benefits and costs to hosts depend on many factors, including host genotype, symbiont species and genotype, and environmental conditions. Here, we present a study demonstrating genotype-by-genotype (G×G) interactions between multiple species of endosymbionts harboured by an insect, and the first to quantify the relative importance of G×G interactions compared with species interactions in such systems. In the most extensive study to date, we microinjected all possible combinations of five Hamiltonella defensa and five Fukatsuia symbiotica (X-type; PAXS) isolates into the pea aphid, Acyrthosiphon pisum. We applied several ecological challenges: a parasitoid wasp, a fungal pathogen, heat shock, and performance on different host plants. Surprisingly, genetic identity and genotype × genotype interactions explained far more of the phenotypic variation (on average 22% and 31% respectively) than species identity or species interactions (on average 12% and 0.4%, respectively). We determined the costs and benefits associated with co-infection, and how these compared to corresponding single infections. All phenotypes were highly reliant on individual isolates or interactions between isolates of the co-infecting partners. Our findings highlight the importance of exploring the eco-evolutionary consequences of these highly specific interactions in communities of co-inherited species.


2020 ◽  
Author(s):  
Jordann E. Trainor ◽  
KR Pooja ◽  
Nathan T. Mortimer

AbstractThe interactions between Drosophila melanogaster and the parasitoid wasps that infect Drosophila species provide an important model for understanding host-parasite relationships. Following parasitoid infection, D. melanogaster larvae mount a response in which immune cells (hemocytes) form a capsule around the wasp egg, which then melanizes leading to death of the parasitoid. Previous studies have found that host hemocyte load, the number of hemocytes available for the encapsulation response, and the production of lamellocytes, an infection induced hemocyte type, are major determinants of host resistance. Parasitoids have evolved various virulence mechanisms to overcome the immune response of the D. melanogaster host, including both active immune suppression by venom proteins and passive immune evasive mechanisms. We find that a previously undescribed parasitoid species, Asobara sp. AsDen, utilizes an active virulence mechanism to infect D. melanogaster hosts. Asobara sp. AsDen infection inhibits host hemocyte expression of msn, a member of the JNK signaling pathway, which plays a role in lamellocyte production. Asobara sp. AsDen infection restricts the production of lamellocytes as assayed by hemocyte cell morphology and altered msn expression. Our findings suggest that Asobara sp. AsDen venom targets host signaling to suppress immunity.DeclarationsFundingThis work was supported by the National Institute of General Medical Sciences of the National Institutes of Health under Award Number R35GM133760.Availability of data and materialSequence data has been deposited in GenBank under accession # MT498809. Custom BLAST databases are available on request to corresponding author.Authors’ contributionsConceived of or designed study: J.E.T., N.T.M.; Performed research: J.E.T., P.K.; Analyzed data: J.E.T., P.K., N.T.M.; Wrote the paper: J.E.T., P.K., N.T.M.


Author(s):  
Giacomo Zilio ◽  
Louise Solveig Noergaard ◽  
Giovanni Petrucci ◽  
Nathalie Zeballos ◽  
Claire Gougat-Barbera ◽  
...  

Dispersal plays a main role in determining spatial dynamics, and both theory and empirical evidence indicate that evolutionary optima exist for constitutive or plastic dispersal behaviour. Plasticity in dispersal can be influenced by factors both internal (state-dependent) or external (context-dependent) to individuals. Parasitism is interesting in this context, as it can influence both types of host dispersal plasticity: individuals can disperse in response to internal infection status but might also respond to the presence of infected individuals around them. We still know little about the driving evolutionary forces of host dispersal plasticity, but a first requirement is the presence of a genetic basis on which natural selection can act. In this study, we used microcosm dispersal mazes to investigate plastic dispersal of 20 strains of the freshwater protist Paramecium caudatum in response to the bacterial parasite Holospora undulata. We additionally quantified the genetic component of the plastic responses, i.e. the heritability of state- and context-depended dispersal. We found that infection by the parasite can either increase or decrease dispersal of individual strains relative to the uninfected (state-dependent plasticity), and this to be heritable. We also found strain-specific change of dispersal of uninfected Paramecium when exposed to variable infection prevalence (context-dependent plasticity) with very low level of heritability. To our knowledge, this is the first explicit empirical demonstration and quantification of genetic variation of plastic dispersal in a host-parasite system, which could have important implications for meta-population and epidemiological dynamics. We discuss some of the underlying mechanisms of this variation and link our results to the existing theoretical models.


2018 ◽  
Vol 373 (1745) ◽  
pp. 20170101 ◽  
Author(s):  
David J. Civitello ◽  
Brent E. Allman ◽  
Connor Morozumi ◽  
Jason R. Rohr

Anthropogenic resource supplementation can shape wildlife disease directly by altering the traits and densities of hosts and parasites or indirectly by stimulating prey, competitor or predator species. We first assess the direct epidemiological consequences of supplementation, highlighting the similarities and differences between food provisioning and two widespread forms of nutrient input: agricultural fertilization and aquatic nutrient enrichment. We then review an aquatic disease system and a general model to assess whether predator and competitor species can enhance or overturn the direct effects of enrichment. All forms of supplementation can directly affect epidemics by increasing host population size or altering parasite production within hosts, but food provisioning is most likely to aggregate hosts and increase parasite transmission. However, if predators or competitors increase in response to supplementation, they could alter resource-fuelled outbreaks in focal hosts. We recommend identifying the traits of hosts, parasites or interacting species that best predict epidemiological responses to supplementation and evaluating the relative importance of these direct and indirect mechanisms. Theory and experiments should examine the timing of behavioural, physiological and demographic changes for realistic, variable scenarios of supplementation. A more integrative view of resource supplementation and wildlife disease could yield broadly applicable disease management strategies. This article is part of the theme issue ‘Anthropogenic resource subsidies and host–parasite dynamics in wildlife’.


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