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Carrasco, J. L.

Publications and source records attributed to Carrasco, J. L..

4 recordsLinked to original sources

Evolution of virulence of a plant RNA virus in age-diverse host populations

Natural host populations are intrinsically age-structured, and developmental stages differ in susceptibility and within-host dynamics, meaning age compositions can impose distinct selective pressure on pathogens. However, how host age structure shapes viral evolution remains largely untested. We experimentally evolved turnip mosaic virus (TuMV) for five passages in Arabidopsis thaliana populations spanning seven demographic regimes (from juvenile-dominated to mature-dominated cohorts). We quantified disease progression, symptom severity and viral load, cross-inoculated evolved lineages across host stages to build quantitative infection matrices, and performed whole-population sequencing at passages 1 and 5 to infer selection coefficients and test for parallelism. Disease traits changed strongly with passage, demography, and their interaction. Disease progression evolved faster in older host populations, whereas severity showed no detectable dependence on median age, implying demographic reweighting of virulence components. Viral load increased through passages and positively correlated with severity, linking within-host fitness to symptoms. Cross-assays revealed a non-nested but modular infection network: juvenile-evolved lineages specialized on pre-bolting plants, whereas lineages from intermediate/older demographies were more stage-generalist. Genomically, both parallel and demography-specific solutions emerged, with a dense cluster of recurrent changes in VPg and several synonymous variants showing consistent or sign-flipping selection across demographies. In conclusion, host age structure is a primary ecological driver of virulence evolution, determining whether viruses evolve faster disease timing versus stronger severity, and whether they specialize or generalize across host stages. These results integrate phenotypes with genome-level responses and suggest that manipulating crop age pyramids could steer virus evolution toward less damaging outcomes.

evolutionary biology↗

Adaptation of turnip mosaic virus to Arabidopsis thaliana involves rewiring of VPg - host proteome interactions

The outcome of a viral infection depends on a complex interplay between the host physiology and the virus, mediated through numerous protein-protein interactions. In a previous study we used high-throughput yeast two-hybrid (HT-Y2H) to identify proteins in Arabidopsis thaliana that bind to the proteins encoded by the turnip mosaic virus (TuMV) genome. Furthermore, after experimental evolution of TuMV lineages in plants with mutations in defense-related or proviral genes, most mutations observed in the evolved viruses affected the VPg cistron. Among these mutations, D113G was a convergent mutation selected in many lineages across different plant genotypes. In contrast, mutation R118H specifically emerged in the jin1 mutant with affected jasmonate signaling. Using the HT-Y2H system, we analyzed the impact of these two mutations on VPgs interaction with plant proteins. Interestingly, both mutations severely compromised the interaction of VPg with the translation initiation factor eIF(iso)4E, a crucial interactor for potyvirus infection. Moreover, mutation D113G, but not R118H, adversely affected the interaction with RHD1, a zinc-finger homeodomain transcription factor involved in regulating DNA demethylation. Our results suggest that RHD1 enhances plant tolerance to TuMV infection.

evolutionary biology↗

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↗

Exploring the role of cellular homologous of the 30K-superfamily of plant virus movement proteins

Genes orthologous to the 30K-superfamily of movement proteins (MP) from plant viruses have been recently discovered by bioinformatics analyses as integrated elements in the genome of most vascular plants. However, their functional relevance for plants is still unclear. Here, we undertake some preliminary steps into the functional characterization of one of these putative MP genes found in Arabidopsis thaliana. We found that the AtMP gene is expressed at different stages of the plant development, with accumulation being highest in flowers but lowest in mature siliques. We also found down-regulation of the gene may result in a small delay in plant development and in an exacerbation of the negative effect of salinity in germination efficiency. We have also explored whether changes in expression of the endogenous AtMP have any effect on susceptibility to infection with several viruses, and found that the infectivity of tobacco rattle tobravirus was strongly dependent on the expression of the endogenous AtMP. Finally, we have cloned the endogenous MP from four different plant species into an expression vector that allows for specifically assessing their activity as cell-to-cell movement proteins and have shown that though some may still retain the ancestral activity, they do so in a quite inefficient manner, thus suggesting they have acquired a novel function during adaptation to the host genome.

evolutionary biology↗