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Correa, R. L.

Publications and source records attributed to Correa, R. L..

3 recordsLinked to original sources

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↗

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↗

Viral fitness determines the magnitude of transcriptomic and epigenomic reprogramming of defense responses in plants

Although epigenetic factors may influence the expression of defense genes in plants, their role in antiviral responses and the impact of viral adaptation and evolution in shaping these interactions are still poorly explored. We used two isolates of turnip mosaic potyvirus (TuMV) with varying degrees of adaptation to Arabidopsis thaliana to address these issues. One of the isolates was experimentally evolved in the plant and presented increased load and virulence relative to the ancestral isolate. The magnitude of the transcriptomic responses were larger for the evolved isolate and indicated a role of innate immunity systems triggered by molecular patterns and effectors in the infection process. Several transposable elements (TEs) located in different chromatin contexts and epigenetic-related genes were also affected. Correspondingly, mutant plants having loss or gain of repressive marks were, respectively, more tolerant and susceptible to TuMV, with a more efficient response against the ancestral isolate. In wild-type plants both isolates induced similar levels of cytosine methylation changes, including in and around TEs and stress-related genes. Results collectively suggested that apart from RNA silencing and basal immunity systems, DNA methylation and histone modification pathways may also be required for mounting proper antiviral defenses in plants and that the effectiveness of this type of regulation strongly depends on the degree of viral adaptation to the host.

evolutionary biology↗