Viruses are the most abundant entities on Earth and have a great capacity for evolution and adaptation. Some viruses are able to infect a wide range of hosts causing damage in a number of important plants while others infect one host species really well and cause severe detrimental symptoms in a short time span. With time viruses can adapt well to novel hosts and increase their infectivity, virulence and therefore provoke more damage to the host. Yet we still lack knowledge about how plants respond to viral infection with viruses that have different adaptation histories or host ranges, or how viruses that are differently adapted to the host respond to distinct environmental challenges. This thesis tried to answer these questions with the help of turnip mosaic virus (TuMV) and plant host Arabidopsis thaliana. Four different strains of TuMV were used; two with different adaptation histories (1) one naïve to arabidopsis, (2) one preadapted to arabidopsis, and two with different host ranges (3) a virus able to infect different genotypes of arabidopsis equally well (generalist) and (4) a virus able to infect only one specific genotype of arabidopsis well (specialist). In the first experiment, a method called genome-wide association studies (GWAS) was used to associate arabidopsis genes involved in viral infection with the naïve and preadapted TuMV strains. Shared and specific host genes for the naïve or preadapted viruses were identified as potential drivers/targets of viral adaptation. Their role in infection was further corroborated with the help of loss-of- function (LOF) mutants. Gene AT2G14080 showed a strong potential role in resistance to pathogens in arabidopsis. In the second experiment, using the same GWAS method, arabidopsis genes that responded differentially to a generalist and a specialist virus were identified and characterized. The generalist virus manipulated a similar set of host genes in order to infect a wide host range successfully. While the specialist virus manipulated more heterogeneous genes because of host-specific selective pressures that modulated the evolution of the specialist virus. Selected genes were characterized further with the help of LOF mutants. In the final experiment, arabidopsis was inoculated with the naïve and preadapted virus and their genetic robustness (the constancy of the phenotype under mutational changes) and environmental robustness (the constancy of the phenotype under environmental changes) were tested. In agreement with the plastogenetic congruence hypothesis, mutational and environmental robustnesses went hand by hand: the naïve virus proved to be more robust both to mutational and environmental perturbations than the preadapted one. These results show how adaptation to one environment limits evolvability in alternative ones, thus restricting the capacity of the preadapted virus to quickly respond to future changes in temperature.

Viruses are the most abundant entities on Earth and have a great capacity for evolution and adaptation. Some viruses are able to infect a wide range of hosts causing damage in a number of important plants while others infect one host species really well and cause severe detrimental symptoms in a short time span. With time viruses can adapt well to novel hosts and increase their infectivity, virulence and therefore provoke more damage to the host. Yet we still lack knowledge about how plants respond to viral infection with viruses that have different adaptation histories or host ranges, or how viruses that are differently adapted to the host respond to distinct environmental challenges. This thesis tried to answer these questions with the help of turnip mosaic virus (TuMV) and plant host Arabidopsis thaliana. Four different strains of TuMV were used; two with different adaptation histories (1) one naïve to arabidopsis, (2) one preadapted to arabidopsis, and two with different host ranges (3) a virus able to infect different genotypes of arabidopsis equally well (generalist) and (4) a virus able to infect only one specific genotype of arabidopsis well (specialist). In the first experiment, a method called genome-wide association studies (GWAS) was used to associate arabidopsis genes involved in viral infection with the naïve and preadapted TuMV strains. Shared and specific host genes for the naïve or preadapted viruses were identified as potential drivers/targets of viral adaptation. Their role in infection was further corroborated with the help of loss-of- function (LOF) mutants. Gene AT2G14080 showed a strong potential role in resistance to pathogens in arabidopsis. In the second experiment, using the same GWAS method, arabidopsis genes that responded differentially to a generalist and a specialist virus were identified and characterized. The generalist virus manipulated a similar set of host genes in order to infect a wide host range successfully. While the specialist virus manipulated more heterogeneous genes because of host-specific selective pressures that modulated the evolution of the specialist virus. Selected genes were characterized further with the help of LOF mutants. In the final experiment, arabidopsis was inoculated with the naïve and preadapted virus and their genetic robustness (the constancy of the phenotype under mutational changes) and environmental robustness (the constancy of the phenotype under environmental changes) were tested. In agreement with the plastogenetic congruence hypothesis, mutational and environmental robustnesses went hand by hand: the naïve virus proved to be more robust both to mutational and environmental perturbations than the preadapted one. These results show how adaptation to one environment limits evolvability in alternative ones, thus restricting the capacity of the preadapted virus to quickly respond to future changes in temperature.