scholarly journals Evolution of phenotypic fluctuation under host-parasite interactions

2021 ◽  
Vol 17 (11) ◽  
pp. e1008694
Author(s):  
Naoto Nishiura ◽  
Kunihiko Kaneko
Keyword(s):  
Gene Expression ◽  
Species Interactions ◽  
Species Interaction ◽  
Phenotypic Variance ◽  
Variable Environment ◽  
Host Parasite Interactions ◽  
Variable Environments ◽  
Single Host ◽  
Sufficient Degree ◽  
Host Parasite

Robustness and plasticity are essential features that allow biological systems to cope with complex and variable environments. In a constant environment, robustness, i.e., insensitivity of phenotypes, is expected to increase, whereas plasticity, i.e., the changeability of phenotypes, tends to diminish. Under a variable environment, existence of plasticity will be relevant. The robustness and plasticity, on the other hand, are related to phenotypic variances. As phenotypic variances decrease with the increase in robustness to perturbations, they are expected to decrease through the evolution. However, in nature, phenotypic fluctuation is preserved to a certain degree. One possible cause for this is environmental variation, where one of the most important “environmental” factors will be inter-species interactions. As a first step toward investigating phenotypic fluctuation in response to an inter-species interaction, we present the study of a simple two-species system that comprises hosts and parasites. Hosts are expected to evolve to achieve a phenotype that optimizes fitness. Then, the robustness of the corresponding phenotype will be increased by reducing phenotypic fluctuations. Conversely, plasticity tends to evolve to avoid certain phenotypes that are attacked by parasites. By using a dynamic model of gene expression for the host, we investigate the evolution of the genotype-phenotype map and of phenotypic variances. If the host–parasite interaction is weak, the fittest phenotype of the host evolves to reduce phenotypic variances. In contrast, if there exists a sufficient degree of interaction, the phenotypic variances of hosts increase to escape parasite attacks. For the latter case, we found two strategies: if the noise in the stochastic gene expression is below a certain threshold, the phenotypic variance increases via genetic diversification, whereas above this threshold, it is increased mediated by noise-induced phenotypic fluctuation. We examine how the increase in the phenotypic variances caused by parasite interactions influences the growth rate of a single host, and observed a trade-off between the two. Our results help elucidate the roles played by noise and genetic mutations in the evolution of phenotypic fluctuation and robustness in response to host–parasite interactions.

scholarly journals Evolution of Phenotypic Plasticity under Host-Parasite Interactions

2021 ◽  
Author(s):  
Naoto Nishiura ◽  
Kunihiko Kaneko
Keyword(s):  
Gene Expression ◽  
Phenotypic Plasticity ◽  
Species Interactions ◽  
Phenotypic Variability ◽  
Biological Systems ◽  
Computer Experiments ◽  
Phenotypic Variance ◽  
Host Parasite Interactions ◽  
Gene Expression Dynamics ◽  
Host Parasite

AbstractRobustness and plasticity are essential features that allow biological systems to cope with complex and variable environments. Through the evolution of a given environment, the former, the insensitivity of phenotypes, is expected to increase, whereas the latter, the changeability of phenotypes, tends to diminish. However, in nature, plasticity is preserved to a certain degree. One possible cause for this is environmental variation, with one of the most important “environmental ” factors being inter-species interactions. As a first step toward investigating phenotypic plasticity in response to an ecological interaction, we present the study of a simple two-species system consisting of hosts and parasites. Hosts are expected to evolve to achieve a phenotype that optimizes fitness and increases the robustness of the corresponding phenotype by reducing phenotypic fluctuations. Conversely, plasticity evolves in order to avoid certain phenotypes being attacked by parasites. By simulating evolution using the host gene-expression dynamics model, we analyze the evolution of genotype-phenotype mapping. If the interaction is weak, the fittest phenotype of the host evolves to reduce phenotypic variances. In contrast, if a sufficient degree of interaction occurs, the phenotypic variances of hosts increase to escape parasite attacks. For the latter case, we found two strategies: if the noise in the stochastic gene expression is below a certain threshold, the phenotypic variance increases via genetic diversification, whereas above the threshold, it is increased due to noise-induced phenotypic plasticity. We examine how the increase in the phenotypic variances due to parasite interactions influences the growth rate of a single host, and observed a trade-off between the two. Our results help elucidate the roles played by noise and genetic mutations in the evolution of phenotypic plasticity and robustness in response to host-parasite interactions.Author summaryPlasticity and phenotypic variability induced by internal or external perturbations are common features of biological systems. However, certain environmental conditions initiate evolution to increase fitness and, in such cases, phenotypic variability is not advantageous, as has been demonstrated by previous laboratory and computer experiments. As a possible origin for such plasticity, we investigated the role of host-parasite interactions, such as those between bacteria and phages. Different parasite types attack hosts of certain phenotypes. Through numerical simulations of the evolution of host genotype-phenotype mapping, we found that, if the interaction is sufficiently strong, hosts increase phenotypic plasticity by increasing phenotypic fluctuations. Depending on the degree of noise in gene expression dynamics, there are two distinct strategies for increasing the phenotypic variances: via stochasticity in gene expression or via genetic variances. The former strategy, which can work over a faster time scale, leads to a decline in fitness, whereas the latter reduces the robustness of the fitted state. Our results provide insights into how phenotypic variances are preserved and how hosts can escape being attacked by parasites whose genes mutate to adapt to changes in parasites. These two host strategies, which depend on internal and external conditions, can be verified experimentally, for example, via the transcriptome analysis of microorganisms.

scholarly journals Annual environmental variation influences host tolerance to parasites

2019 ◽  
Vol 286 (1897) ◽  
pp. 20190049 ◽  
Author(s):  
Sabrina M. McNew ◽  
Sarah A. Knutie ◽  
Graham B. Goodman ◽  
Angela Theodosopoulos ◽  
Ashley Saulsberry ◽  
...  
Keyword(s):  
Environmental Conditions ◽  
Environmental Variation ◽  
Host Population ◽  
Variable Environment ◽  
Host Parasite Interactions ◽  
Video Observations ◽  
Single Host ◽  
Parental Provisioning ◽  
Host Tolerance ◽  
Host Parasite

When confronted with a parasite or pathogen, hosts can defend themselves by resisting or tolerating the attack. While resistance can be diminished when resources are limited, it is unclear how robust tolerance is to changes in environmental conditions. Here, we investigate the sensitivity of tolerance in a single host population living in a highly variable environment. We manipulated the abundance of an invasive parasitic fly, Philornis downsi , in nests of Galápagos mockingbirds ( Mimus parvulus ) over four field seasons and measured host fitness in response to parasitism. Mockingbird tolerance to P. downsi varied significantly among years and decreased when rainfall was limited. Video observations indicate that parental provisioning of nestlings appears key to tolerance: in drought years, mockingbirds likely do not have sufficient resources to compensate for the effects of P. downsi . These results indicate that host tolerance is a labile trait and suggest that environmental variation plays a major role in mediating the consequences of host–parasite interactions.

scholarly journals A Primer on Predicting Species Interaction Networks (Across Space and Time)

2021 ◽  
Author(s):  
Tanya Strydom ◽  
Michael David Catchen ◽  
Francis Banville ◽  
Dominique Caron ◽  
Gabriel Dansereau ◽  
...  
Keyword(s):  
Species Interactions ◽  
Species Interaction ◽  
Multiple Sources ◽  
Modeling Tools ◽  
Structure Variation ◽  
Road Map ◽  
Host Parasite Interactions ◽  
Challenges And Opportunities ◽  
Simple Neural Network ◽  
Host Parasite

Networks of species interactions can capture meaningful information on the structure and functioning of ecosystems. Yet the scarcity of existing data, and the difficulty associated with comprehensively sampling interactions between species, means that to describe the structure, variation, and change of ecological networks over time and space, we need to rely on modeling tools with the capacity to make accurate predictions about how species interact. Here we provide a proof-of-concept, where we show a simple neural-network model makes accurate predictions about species interactions, and use this model to reconstruct a metaweb of host-parasite interactions across space, and assess the challenges and opportunities associated with improving interaction predictions. We then provide a primer on the relevant method and tools that will guide the development and integration of these tools, and provide a road map forward toward integration of multiple sources of data and methodlogical approaches (including statistical, dynamical, and inferential models) to sketch the path forward for this research program.

scholarly journals Transcriptome of the parasitic flatworm Schistosoma mansoni during intra-mammalian development

2019 ◽  
Author(s):  
Arporn Wangwiwatsin ◽  
Anna V. Protasio ◽  
Shona Wilson ◽  
Christian Owusu ◽  
Nancy E. Holroyd ◽  
...  
Keyword(s):  
Gene Expression ◽  
Schistosoma Mansoni ◽  
Chronic Infection ◽  
Egg Laying ◽  
Mammalian Host ◽  
Expression Data ◽  
Mammalian Development ◽  
Host Parasite Interactions ◽  
Parasitic Flatworm ◽  
Host Parasite

AbstractSchistosomes are parasitic blood flukes that survive for many years within the mammalian host vasculature. How the parasites establish a chronic infection in the hostile bloodstream environment, whilst evading the host immune response is poorly understood. The parasite develops morphologically and grows as it migrates to its preferred vascular niche, avoiding or repairing damage from the host immune system. In this study, we investigated temporal changes in gene expression during the intra-mammalian development of Schistosoma mansoni. RNA-seq data were analysed from parasites developing in the lung through to egg-laying mature adult worms, providing a comprehensive picture of in vivo intra-mammalian development. Remarkably, genes involved in signalling pathways, developmental control, and adaptation to oxidative stress were up-regulated in the lung stage. The data also suggested a potential role in immune evasion for a previously uncharacterised gene. This study not only provides a large and comprehensive data resource for the research community, but also reveals new directions for further characterising host–parasite interactions that could ultimately lead to new control strategies for this neglected tropical disease pathogen.Author SummaryThe life cycle of the parasitic flatworm Schistosoma mansoni is split between snail and mammalian (often human) hosts. An infection can last for more than 10 years, during which time the parasite physically interacts with its mammalian host as it moves through the bloodstream, travelling through the lungs and liver, to eventually establish a chronic infection in the blood vessels around the host gut. Throughout this complex journey, the parasite develops from a relatively simple larval form into a more complex, sexually reproducing adult. To understand the molecular basis of parasite interactions with the host during this complex journey we have produced genome-wide expression data from developing parasites. The parasites were collected from experimentally-infected mice over its developmental time-course from the poorly studied lung stage, to the fully mature egg-laying adult worm. The data highlight many genes involved in processes known to be associated with key stages of the infection. In addition, the gene expression data provide a unique view of interactions between the parasite and the immune system in the lung, including novel players in host-parasite interactions. A detailed understanding of these processes may provide new opportunities to design intervention strategies, particularly those focussed on the early stages of the infection that are not targeted by current chemotherapy.

The risk of use small matrices to measure specialization in host–parasite interaction networks: a comment to Rivera-García et al. (2016)

Parasitology ◽  
2017 ◽  
Vol 144 (8) ◽  
pp. 1102-1106 ◽  
Author(s):  
PEDRO LUNA ◽  
ERICK J. CORRO ◽  
DIANA A. AHUATZIN-FLORES ◽  
REUBER L. ANTONIAZZI ◽  
NATHALIA BARROZO ◽  
...  
Keyword(s):  
Species Richness ◽  
Species Interactions ◽  
Simulated Data ◽  
Interaction Networks ◽  
Host Parasite Interactions ◽  
The Matrix ◽  
Bat Fly ◽  
Host Parasite

SUMMARYIn the last years, there were a growing number of studies using the metric H2′ to calculate complementary specialization in host–parasite interaction networks. However, only a few studies have explored the sensitivity of H2′ to network dimensions (i.e. species richness and number of interactions), which consequently could generate studies that are not comparable among them or lead to biased conclusions. In this study, we used the recent published study conducted by Rivera-García et al. in 2016 involving host–bat fly networks as an example to call attention to the risk of using H2′ to calculate specialization for small matrices. After conducting analyses based on both empirical and simulated data, we show that H2′ values are strongly affected by randomly allocation of species interactions to another cell in the matrix for small networks and that therefore the results and conclusions presented in Rivera-García et al. in 2016 are only an artefact of the dataset used. Therefore, we fully recommended taking into account the careful use of small networks to measuring specialization in host–parasite interactions.

scholarly journals Symbiont-conferred immunity interacts with the effects of parasitoid genotype and intraguild predation to shape pea aphid immunity in a clone-specific fashion

2021 ◽  
Author(s):  
Samuel Alexander Purkiss ◽  
Mouhammad Shadi Khudr ◽  
Oscar Enrique Aguinaga ◽  
Reinmar Hager
Keyword(s):  
Genetic Variation ◽  
Intraguild Predation ◽  
Species Interactions ◽  
Acyrthosiphon Pisum ◽  
Species Interaction ◽  
Genetic Effects ◽  
Pea Aphid ◽  
Aphidius Ervi ◽  
Indirect Genetic Effects ◽  
Host Parasite

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.

scholarly journals A test of the Baldwin Effect: Differences in both constitutive expression and inducible responses to parasites underlie variation in host response to a parasite

2020 ◽  
Author(s):  
Lauren Fuess ◽  
Jesse N. Weber ◽  
Stijn den Haan ◽  
Natalie C. Steinel ◽  
Kum Chuan Shim ◽  
...  
Keyword(s):  
Gene Expression ◽  
Host Resistance ◽  
Gasterosteus Aculeatus ◽  
Constitutive Expression ◽  
Baldwin Effect ◽  
Data Set ◽  
Host Parasite Interactions ◽  
Evolution Of Resistance ◽  
Host Parasite ◽  
The Baldwin Effect

ABSTRACTDespite the significant effect of host-parasite interactions on both ecological systems and organism health, there is still limited understanding of the mechanisms driving evolution of host resistance to parasites. One model of rapid evolution, the Baldwin Effect, describes the role of plasticity in adaptation to novel conditions, and subsequent canalization of associated traits. While mostly applied in the context of environmental conditions, this theory may be relevant to the evolution of host resistance to novel parasites. Here we test the applicability of the Baldwin Effect to the evolution of resistance in a natural system using threespine stickleback fish (Gasterosteus aculeatus) and their cestode parasite Schistochephalus solidus. We leverage a large transcriptomic data set to describe the response to S. solidus infection by three different genetic crosses of stickleback, from a resistant and a tolerant population. Hosts mount a multigenic response to the parasite that is similar among host genotypes. In addition, we document extensive constitutive variation in gene expression among host genotypes. However, although many genes are both infection-induced and differentially expressed between genotypes, this overlap is not more extensive than expected by chance. We also see little evidence of canalization of infection-induced gene expression in the derived resistant population. These patterns do not support the Baldwin Effect, though they illustrate the importance of variation in both constitutive expression and induced responses to parasites. Finally, our results improve understanding of the cellular mechanisms underlying a putative resistance phenotype (fibrosis). Combined, our results highlight the importance of both constitutive and inducible variation in the evolution of resistance to parasites, and identify new target genes contributing to fibrosis. These findings advance understanding of host-parasite interactions and co-evolutionary relationships in natural systems.

scholarly journals Host–Parasite Interactions and the Evolution of Gene Expression

PLoS Biology ◽  
2005 ◽  
Vol 3 (7) ◽  
pp. e203 ◽  
Author(s):  
Scott L Nuismer ◽  
Sarah P Otto
Keyword(s):  
Gene Expression ◽  
Host Parasite Interactions ◽  
Host Parasite

scholarly journals Dual RNA Sequencing Meta-analysis in Plasmodium Infection Identifies Host-Parasite Interactions

mSystems ◽  
2021 ◽  
Vol 6 (2) ◽  
Author(s):  
Parnika Mukherjee ◽  
Gaétan Burgio ◽  
Emanuel Heitlinger
Keyword(s):  
Gene Expression ◽  
Rna Sequencing ◽  
Laboratory Experiments ◽  
Meta Analysis ◽  
Model Systems ◽  
Rna Seq ◽  
Content Type ◽  
Human Malaria ◽  
Host Parasite Interactions ◽  
Host Parasite

ABSTRACT Dual RNA sequencing (RNA-Seq) is the simultaneous transcriptomic analysis of interacting symbionts, for example, in malaria. Potential cross-species interactions identified by correlated gene expression might highlight interlinked signaling, metabolic, or gene regulatory pathways in addition to physically interacting proteins. Often, malaria studies address one of the interacting organisms—host or parasite—rendering the other “contamination.” Here we perform a meta-analysis using such studies for cross-species expression analysis. We screened experiments for gene expression from host and Plasmodium. Out of 171 studies in Homo sapiens, Macaca mulatta, and Mus musculus, we identified 63 potential studies containing host and parasite data. While 16 studies (1,950 samples) explicitly performed dual RNA-Seq, 47 (1,398 samples) originally focused on one organism. We found 915 experimental replicates from 20 blood studies to be suitable for coexpression analysis and used orthologs for meta-analysis across different host-parasite systems. Centrality metrics from the derived gene expression networks correlated with gene essentiality in the parasites. We found indications of host immune response to elements of the Plasmodium protein degradation system, an antimalarial drug target. We identified well-studied immune responses in the host with our coexpression networks, as our approach recovers known broad processes interlinked between hosts and parasites in addition to individual host and parasite protein associations. The set of core interactions represents commonalities between human malaria and its model systems for prioritization in laboratory experiments. Our approach might also allow insights into the transferability of model systems for different pathways in malaria studies. IMPORTANCE Malaria still causes about 400,000 deaths a year and is one of the most studied infectious diseases. The disease is studied in mice and monkeys as lab models to derive potential therapeutic intervention in human malaria. Interactions between Plasmodium spp. and its hosts are either conserved across different host-parasite systems or idiosyncratic to those systems. Here we use correlation of gene expression from different RNA-Seq studies to infer common host-parasite interactions across human, mouse, and monkey studies. First, we find a set of very conserved interactors, worth further scrutiny in focused laboratory experiments. Second, this work might help assess to which extent experiments and knowledge on different pathways can be transferred from models to humans for potential therapy.

scholarly journals Large, rapidly evolving gene families are at the forefront of host–parasite interactions inApicomplexa

Parasitology ◽  
2014 ◽  
Vol 142 (S1) ◽  
pp. S57-S70 ◽  
Author(s):  
ADAM J REID
Keyword(s):  
Gene Expression ◽  
Malaria Parasite ◽  
Gene Expression Regulation ◽  
Protein Localization ◽  
Animal Health ◽  
Gene Families ◽  
Sequence Diversity ◽  
Genomic Context ◽  
Host Parasite Interactions ◽  
Host Parasite

SUMMARYTheApicomplexais a phylum of parasitic protozoa, which includes the malaria parasitePlasmodium, amongst other species that can devastate human and animal health. The past decade has seen the release of genome sequences for many of the most important apicomplexan species, providing an excellent basis for improving our understanding of their biology. One of the key features of each genome is a unique set of large, variant gene families. Although closely related species share the same families, even different types of malaria parasite have distinct families. In some species they tend to be found at the ends of chromosomes, which may facilitate aspects of gene expression regulation and generation of sequence diversity. In others they are scattered apparently randomly across chromosomes. For some families there is evidence they are involved in antigenic variation, immune regulation and immune evasion. For others there are no known functions. Even where function is unknown these families are most often predicted to be exposed to the host, contain much sequence diversity and evolve rapidly. Based on these properties it is clear that they are at the forefront of host–parasite interactions. In this review I compare and contrast the genomic context, gene structure, gene expression, protein localization and function of these families across different species.

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