Instituto de Biología Integrativa de Sistemas (I 2 SysBio), CSIC-Universitat de València, Catedrático Agustín Escardino 9, Paterna, Valencia, 46980, Spain.
Departmento de Genética, Universidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro, Brazil.
BMC Genomics. 2024 Sep 30;25(1):897. doi: 10.1186/s12864-024-10798-x.
Plant-virus interaction models propose that a virus's 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 plant's resistance genes.
植物-病毒相互作用模型提出，病毒感染宿主基因型的能力取决于毒力和抗性基因之间的兼容性。最近，我们进行了一项进化实验，其中芜菁花叶病毒（TuMV）的系在携带 DNA 甲基化和组蛋白去甲基化表观遗传途径组分突变的拟南芥基因型中传代。所有进化的系都以宿主基因型依赖的方式增加了感染性、毒力和病毒载量。
为了更好地理解这些进化关系的潜在原因，我们深入研究了突变和 WT 植物基因型在模拟条件下和感染祖先或进化病毒时的转录组响应。这种比较使我们能够将每个基因分类为九个基本表达谱。关于病毒适应的靶标，我们的分析允许识别共同的病毒靶标以及宿主基因型特异性基因和生物过程类别。正如预期的那样，感染后发现与免疫反应相关的基因发生了改变。然而，我们还注意到其他功能组的普遍过度表达，这表明病毒适应不仅仅是由植物抗性基因的表达水平驱动的。此外，在差异表达基因内或上游存在转座元件与差异表达之间存在显著关联。最后，将转录组数据整合到病毒-宿主蛋白质-蛋白质相互作用网络中突出了最具影响力的相互作用。
这些发现进一步阐明了植物和病毒之间的复杂动态，表明病毒的感染力取决于除植物抗性基因之外的各种因素。
