Transcriptomic analysis of interplay between Arabidopsis developmental stages and TuMV infection
Gene expression patterns differ throughout an organism lifetime, since biological needs and goals change as individuals grow and age. These changes on gene expression may imply changes in immune defense responses, and therefore organisms may present different susceptibilities to pathogen infection depending on the life moment they are infected at. In plants, some studies support the notion that infections are less severe in aged than in younger individuals, which is consequence of a plant defense response known as age related resistance (ARR). However, little is known about whether ARR is also effective against viruses. To characterize how developmental stages may affect the outcome of a viral infection and study the host differential strategies and responses to it, we used the pathosystem Arabidopsis thaliana - turnip mosaic virus (TuMV) at three different host developmental stages: juvenile vegetative, bolting (transition from vegetative to reproductive) and mature reproductive. For that, we inoculated and experimentally evolved two viral strains of TuMV: one naive and other well-adapted to Arabidopsis on each developmental stage. For both viral strains, we observed that the infection was faster and more severe as hosts grew older. After the evolution, we also observed a link between virulence and age: while all evolved viruses caused a significant reduction on seed progression, hosts infected on a stage of reproductive growth produced significantly more offspring than those infected on the other two developmental stages. Next, we characterized the hosts transcriptional responses to viral infection on all developmental stages, finding that even though the biological processes involved on the response against all evolved viruses were similar, hormone levels in conjunction with the regulation of a particular set of genes ought to be the reason responsible for this age-dependent susceptibility to viral infection. Specifically, we hypothesize that abscisic acid may be a key component on these processes. Overall, our study contributes to understand the impact of host age upon the responses to viral infection and tries to shed light on the molecular mechanisms behind it.