Biology subjects

Ambros, S.

Publications and source records attributed to Ambros, S..

7 recordsLinked to original sources

bioRxiv2025

Host replacement dynamics shape virulence and genome evolution in a plant RNA virus

We have investigated how the dynamics of host replacement affect the evolution of a plant RNA virus. Specifically, we have examined how sudden vs. gradual transitions from more susceptible to less susceptible Arabidopsis thaliana genotypes influence turnip mosaic virus virulence and population genomic diversity. Our results show that the evolution of virulence and the complexity of the mutant swarm is linked to both the type of host succession and the genetic basis of the host resistance. Faster changes in virulence are observed after sudden transitions, with an evolutionary trend towards more severe symptoms that appear later during infection. Gradual transitions resulted in greater population mutational load and higher genetic polymorphism compared to sudden transitions. In contrast, beneficial mutations associated with sudden transitions had stronger fitness effects than those linked to gradual transitions. This research highlights the importance of considering the rate of environmental changes in virus evolution and provides insights into predicting how viruses adapt and evolve in temporally changing environments, with implications for agriculture and public health.

evolutionary biology↗

bioRxiv2024

Transcriptomic Insights into the Epigenetic Modulation of Turnip Mosaic Virus Evolution in Arabidopsis thaliana

Plant-virus interaction models propose that a viruss ability to infect a host genotype depends on the compatibility between virulence and resistance genes. Recently, we conducted an evolution experiment in which lineages of turnip mosaic virus (TuMV) were passaged in Arabidopsis thaliana genotypes carrying mutations in components of the DNA methylation and the histone demethylation epigenetic pathways. All evolved lineages increased infectivity, virulence and viral load in a host genotype-dependent manner. To better understand the underlying reasons for these evolved relationships, we delved into the transcriptomic responses of mutant and WT plant genotypes in mock conditions and infected with either the ancestral or evolved viruses. Such a comparison allowed us to classify every gene into nine basic expression profiles. Regarding the targets of viral adaptation, our analyses allowed the identification of common viral targets as well as host genotype-specific genes and categories of biological processes. As expected, immune response-related genes were found to be altered upon infection. However, we also noticed the pervasive over-representation of other functional groups, suggesting that viral adaptation was not solely driven by the level of expression of plant resistance genes. In addition, a significant association between the presence of transposable elements within or upstream the differentially expressed genes was observed. Finally, integration of transcriptomic data into a virus-host protein-protein interaction network highlighted the most impactful interactions. These findings shed extra light on the complex dynamics between plants and viruses, indicating that viral infectivity depends on various factors beyond just the plants resistance genes.

evolutionary biology↗

bioRxiv2023

Phenotypic and genomic changes during Turnip mosaic virus adaptation to Arabidopsis thaliana mutants lacking epigenetic regulatory factors

In this study we investigated how RNA viral populations evolve, interact and adapt to epigenetically-controlled plant defense mechanisms. We have evolved five independent lineages of turnip mosaic virus (TuMV) in a set of Arabidopsis thaliana genotypes carrying mutations that influence important elements of two main epigenetic pathways. All evolved lineages showed adaptation to the lack of epigenetically-regulated responses through significant increases in infectivity, virulence and viral load although the magnitude of the improvements strongly depended on the plant genotype. In early passages, these traits evolved more rapidly, but the rate of evolution flattened out in later ones. Viral load was positively correlated with different measures of virulence, though the strength of the associations changed from the ancestral to the evolved viruses. High-throughput sequencing was used to evaluate the viral diversity of each lineage, as well as characterizing the nature of fixed mutations, evolutionary convergences and potential targets of TuMV adaptation. Within each lineage, we observed a net increase in genome-wide genetic diversity, with some instances where nonsynonymous alleles experienced a transient rise in abundance before being displaced by the ancestral allele. Viral VPg protein has been shown as a key player in the adaptation process, even though no obvious association between fixed alleles and host genotype was found. Layman SummaryEpigenetic factors influence the expression of defense genes in plants, allowing for phenotypic rapid responses to infections by pathogens. The role of epigenetics in shaping the coevolution between host and pathogens has received very little attention. Here, we explored how RNA viruses interact and adapt to plant defense mechanisms that are controlled by epigenetic factors. We conducted evolution experiments on turnip mosaic virus using Arabidopsis thaliana genotypes with mutations that affect epigenetic pathways. We found that all evolved viral lineages adapted to the alteration of epigenetically-regulated responses by becoming more infectious, virulent, and having a higher viral load. The improvements varied depending on the plant genotype. The study also found that viral load was positively correlated with virulence, but the associations changed from the original to the evolved viruses. We used high-throughput sequencing to evaluate viral diversity and found an increase in each evolving lineage. We found that virus adaptation primarily targeted viral VPg, despite no obvious association between fixed alleles and host genotype being found. Teaser TextDiscover how RNA viruses adapt and evolve to plant defense mechanisms controlled by epigenetic factors. This research found that epigenetic regulation of defense genes modulates viral evolution. Viral lineages became more infectious, virulent, and had a higher viral load. Find out more about the correlation between viral load and virulence, viral diversity, and the primary virus genomic target of adaptation.

evolutionary biology↗

bioRxiv2020

Defects in plant immunity modulate the rates and patterns of RNA virus evolution

It is assumed that host genetic variability for susceptibility to infection necessarily conditions virus evolution. Differences in host susceptibility can either drive the virus to diversify into strains that track different defense alleles (e.g., antigenic diversity) or to infect only the most susceptible genotypes. To clarify these processes and their effect on virulence, we have studied how variability in host defense responses determine the evolutionary fate of viruses. To accomplish this, we performed evolution experiments with Turnip mosaic potyvirus in Arabidopsis thaliana mutants. Mutant plants had disruptions in infection-response signaling pathways or in genes whose products are essential for potyvirus infection. Genotypes were classified into five phenogroups according to their response to infection. In order to disentangle how host susceptibility affects virus adaptation, independent viral lineages were evolved in selected plant genotypes. Evaluating disease-related traits of the evolved lineages, we found that evolution proceeded faster in the most resistant hosts than in the most permissive ones, as expected for adaptation to a harsh environment. By sequencing the genomes of the evolved viral lineages, we found that the multifunctional protein VPg turned out to be the target of selection in most host genotypes. When all evolved viral lineages were tested for fitness in all plant genotypes used in the experiments, we found compelling evidences that generalist viruses were selected by the most restrictive plant genotypes, while permissive genotypes selected for specialist viruses. Overall, this work illustrates how different host defense signaling pathways constrain not only disease-related traits but virus evolution.

evolutionary biology↗

bioRxiv2018

Engineered Genetic Redundancy Relaxes Selective Constraints upon Endogenous Genes in Viral RNA Genomes

1Genetic redundancy, understood as the functional overlap of different genes, is a double-edge sword. At the one side, it is thought to serve as a robustness mechanism that buffers the deleterious effect of mutations hitting one of the redundant copies, thus resulting in pseudogenization. At the other side, it is considered as a source of genetic and functional innovation. In any case, genetically redundant genes are expected to show an acceleration in the rate of molecular evolution. Here we tackle the role of genetic redundancy in viral RNA genomes. To this end, we have evaluated the rates of compensatory evolution for deleterious mutations affecting an essential function, the suppression of RNA silencing plant defense, of tobacco etch potyvirus (TEV). TEV genotypes containing deleterious mutations in presence/absence of engineered genetic redundancy were evolved and the pattern of fitness and virulence recovery evaluated. Genetically redundant genotypes suffered less from the effect of deleterious mutations and showed relatively minor changes in fitness and virulence. By contrast, non-genetically redundant genotypes had very low fitness and virulence at the beginning of the evolution experiment that were fully recovered by the end. At the molecular level, the outcome depended on the combination of the actual mutations being compensated and the presence/absence of genetic redundancy. Reversions to wild-type alleles were the norm in the non-redundant genotypes while redundant ones either did not fix any mutation at all or showed a higher nonsynonymous mutational load.

evolutionary biology↗

bioRxiv2017

Diminishing returns of inoculum size on the rate of a plant RNA virus evolution

Understanding how genetic drift, mutation and selection interplay in determining the evolutionary fate of populations is one of the central questions of Evolutionary Biology. Theory predicts that by increasing the number of coexisting beneficial alleles in a population beyond some point does not necessarily translates into an acceleration in the rate of evolution. This diminishing-returns effect of beneficial genetic variability in microbial asexual populations is known as clonal interference. Clonal interference has been shown to operate in experimental populations of animal RNA viruses replicating in cell cultures. Here we carried out experiments to test whether a similar diminishing-returns of population size on the rate of adaptation exists for a plant RNA virus infecting real multicellular hosts. We have performed evolution experiments with tobacco etch potyvirus in two hosts, the natural and a novel one, at different inoculation sizes and estimated the rates of evolution for two phenotypic fitness-related traits. Firstly, we found that evolution proceeds faster in the novel than in the original host. Secondly, we found the predicted diminishing-returns effect of inoculum size on the rate of evolution for one of the fitness traits, but not for the other, which suggests that selection operates differently on each trait.

evolutionary biology↗

bioRxiv2017

Viral fitness predicts the magnitude and direction of perturbations in the infected host transcriptome

Determining the fitness of viral genotypes has become a standard practice in virology as it is essential to evaluate their evolutionary potential. Darwinian fitness, defined as the advantage of a given genotype with respect to a reference one, is a mesoscopic property that captures into a single figure differences in performance at every stage of viral infection. But to which extent viral fitness results from particular molecular interactions with host factors and regulatory networks during infection? Can we identify host genes, and then functional classes, whose expression depends on viral fitness? Here, we compared the transcriptomes of tobacco plants infected with seven genotypes of tobacco etch potyvirus (TEV) that differ in fitness. We found that the larger the fitness differences among genotypes, the more dissimilar the transcriptomic profiles are. Consistently, two different mutations, one in the viral RNA polymerase and another in the viral suppressor of RNA silencing, that led to close fitness values, also resulted in significantly similar gene expression profiles. Moreover, we identified host genes whose expression showed a significant correlation, positive or negative, with TEV fitness. Over-expression of genes with positive correlation activates hormone-and RNA silencing-mediated pathways of plant defense. By contrast, under-expression of genes negatively correlated reduces metabolism, growth, and development. Overall, these results reveal the high information content of viral fitness, and suggest its potential use to predict differences in genomic profiles of infected hosts.

evolutionary biology↗