Defense pathways in Arabidopsis restricting compatible tobamoviruses during infection

Virus infected plants often develop strong disease symptoms including leaf deformation, chlorosis, necrosis and growth inhibition. In agriculture systems virus infection can lead to severe yield losses and a better understanding of plant defenses against viruses is therefore desirable in order for develop new strategies against diseases in crops caused by viruses. Specific resistance to viruses has been studied intensively in the past but host tolerance and recovery have received little attention.
Symptomatic virus infections can persist throughout the life of the host. However, in some cases a recovery from symptoms can be observed. Recovery has been associated with host anti-viral RNA-silencing targeting viral nucleic acids for destructing or inactivation. However, it is well established that compatible viruses suppress RNA-silencing in order to establish and maintain an infection and the exact role of RNA-silencing in onset and maintenance of recovery is therefore unclear. To address this question a “recovery-system” for the tobamovirus Oilseed rape mosaic virus (ORMV) was set up in the model plant Arabidopsis thaliana and characterized (chapter 2). Through the use of Arabidopsis mutants we show that specific RNA-silencing pathways are essential for recovery, included some known to be involved in non-autonomous RNA-silencing. Furthermore, mutants with increased RNA-silencing capacity did recover earlier than wild type plants, suggesting that oscillations in RNA-silencing activity could be involved in the onset of recovery.
RNA-silencing is an important anti-viral defense mechanism but also defense pathways regulated by hormones are induced during compatible virus infections. The changes in gene expression observed upon compatible virus infections are similar to those observed for infection with other biotic plant pathogens, but the importance of virus-induced defense responses is not fully understood. Non-viral plant pathogens predominately live in the apoplast and the presence of pathogen-derived “non-self” molecules is sensed through receptors in the plasma membrane, a mechanism referred to as Pattern-Triggered-Immunity (PTI). It is unclear if intercellular pathogens, such as viruses, can induce defense responses in plants through PTI and if PTI is involved in plant defense against viruses. In this thesis we show that mutants of BAK1; a regulator of many receptors involved in PTI, are hypersuceptible to several RNA viruses (chapter 3). Furthermore crude extracts from virus-infected plants contain compounds that can elicit PTI-responses (chapter 3). Taken together this indicates that virus infections induce PTI through an unidentified, likely plant-derived compound.
Studies of compatible virus infections have focused on plant-virus interactions that lead to disease symptom formation. However, virus infections can progress almost or completely symptomless referred to as tolerance. Mechanisms controlling tolerance to viruses in plants have not been described until now. Infections of Arabidopsis with tobamovirus Tobacco mosaic virus (TMV) progress almost symptomless in most ecotypes. Characterization of TMV infections in tolerant and symptomatic Arabidopsis ecotypes revealed that symptom formation is associated with accelerated viral movement and induction of defense responses (chapter 4). Furthermore is symptom formation independent of RNA-silencing and Salicylic Acid (SA) signaling (chapter 4).