Viral Riders of the Plant’s Defence Storm

Abstract

Several biological phenomena are currently interpreted through changes in transcript abundance, yet plant viruses infection outcome is ultimately determined by posttranscriptional processes that control RNA fate. This thesis investigates how plant viruses exploit host post-transcriptional regulatory mechanisms to promote infection, with particular focus on RNA silencing, biomolecular condensation, translation control, and autophagy-associated immune balancing. The first part of the thesis examines how antiviral RNA silencing influences reproductive fitness and vertical transmission across six phylogenetically diverse Arabidopsis-infecting viruses. Although impairment of major silencing components had limited effects on viral accumulation in vegetative tissues, it strongly altered reproductive outcome. Most viruses caused severe fertility defects when RNA silencing was impaired, whereas Turnip rosette virus showed increased vertical transmission. The second part addresses how double-stranded RNA regulates the multifunctional Cauliflower mosaic virus protein P6. The results support that dsRNA and RNA:DNA hybrids promote P6 condensation into viroplasm-associated structures, and that this transition antagonizes TOR-associated functions linked to translational activation and chlorosis. These findings indicate that viral protein function can be reorganized through changes in physical state, thereby connecting dsRNA, biomolecular condensation, and the functional partitioning of infection processes. The third part shows that host defence activation can itself become a resource for viral infection. In the Turnip crinkle virus pathosystem, salicylic acid promotes viral capindependent translation through the viral untranslated regions, whereas autophagy acts as a balancing mechanism that limits the physiological cost of this defenceassociated state. Thus, immune activation is not necessarily antiviral in outcome but may instead be co-opted to support viral translation. Together, the three studies show that plant virus infection is best understood as a contest over post-transcriptional RNA fate rather than transcript accumulation.