Final Report Summary - IBIS (Identification of Basal Immunity mechanismS against plant pathogenic viruses)
Organisms detect microbes by perceiving pathogen-associated molecular patterns (PAMPs) via pattern recognition receptors (PRRs). PAMP-PRR interaction activates a range of fast and very efficient defense responses leading to PAMP-triggered immunity (PTI). To counteract this defense strategy, successful pathogens deploy effector proteins, the primary function of which is to interfere with PTI. Over the last 15 years, extensive attention has been paid to the identification of PRRs, signalling components, pathogen effectors and their host targets in host-microbe interactions. Nevertheless, no PRRs involved in PTI pathways against viruses has been identified in plants so far. However, converging elements suggest that basal immunity against viruses also exists in plants: i) early host responses following virus infection overlap with the typical PTI responses, including ion fluxes, ROS production, activation of WRKY and MYB transcription factors and induction of specific defense genes, ii) many MAPKs are involved in plant-virus interactions, including MAPK4 that is a key factor in plant basal immunity, iii) BAK1 and its closest paralog BKK1 are clearly involved in plant defense against viruses, and iv) the NIK1 protein, another RLK belonging to the closest subgroup of BAK1 and BKK1 family, has been strongly associated with Arabidopsis antiviral defense and directly targeted by a viral protein during plant infection.
The long-term objective of this project is to understand how plants perceive viruses, and signal immunity towards plant resistance. In this context, the project "IBIS: Identification of Basal Immunity mechanismS against plant pathogenic viruses" aimed at the identification of the cellular processes underlying basal immunity against plant viruses, using the Plum pox virus-Arabidopsis thaliana pathosystem as a model for plant-virus interactions. This broad objective was performed using holistic and interconnected tasks aiming at the evaluation at different levels of the molecular dialog between the virus and its host, through a multidisciplinary project.
The three main objectives of the project IBIS were: i) Identification of cellular components involved in basal immunity against PPV, ii) Functional characterization of PPV effectors suppressing plant basal immunity, and iii) Evaluation of the overlap between the basal immunity pathways triggered by plant pathogens.
In order to determine whether the proteins already identified in plant basal immunity against non-viral pathogens could play also a role in plant resistance to viruses, Arabidopsis reverse genetics analyses have been performed. The results revealed the role of the PTI machinery in Arabidopsis resistance to PPV, strengthening the double hypothesis that plants defend themselves against viruses through basal immunity and that basal immunity pathways against viral pathogens are at least partially shared with basal immunity pathways against non-viral pathogens. In addition, one PPV protein negatively regulates PAMP-triggered responses, revealing for the first time that the genome of plant viruses encode PTI suppressing-pathogenic effectors.
PERSPECTIVE: HOW CAN SCIENCE TRANSLATE PTI-MEDIATED ANTIVIRAL MECHANISMS TOWARDS CROP IMPROVEMENT?
So far, the only powerful strategy to control viral epidemics in field relies on the use of genetic resistances. Crop improvement programs aim at obtaining new resistant varieties, blocking viral multiplication and/or limiting virus-associated damages. Unfortunately, by their inherent nature, viruses evolve very quickly the ability to overcome the resistances employed by breeders. Hence, the extreme genetic plasticity of viruses represents a major challenge for the coming years. The efficiency and durability of resistance mechanisms depend mostly upon the resistance timing of action and the conservation of the pathogen elicitor molecule into the pathogen family. In this context, PTI mechanisms will combine these criteria, as PTI-associated defense reactions are extremely fast and antiviral PTI is triggered by viral nucleic acids (well characterized in the animal field) highly characteristic of viruses. Therefore, translating fundamental knowledge about antiviral PTI mechanisms into crop improvement programs will bring considerable advances in the control of viral epidemics in fields.
The long-term objective of this project is to understand how plants perceive viruses, and signal immunity towards plant resistance. In this context, the project "IBIS: Identification of Basal Immunity mechanismS against plant pathogenic viruses" aimed at the identification of the cellular processes underlying basal immunity against plant viruses, using the Plum pox virus-Arabidopsis thaliana pathosystem as a model for plant-virus interactions. This broad objective was performed using holistic and interconnected tasks aiming at the evaluation at different levels of the molecular dialog between the virus and its host, through a multidisciplinary project.
The three main objectives of the project IBIS were: i) Identification of cellular components involved in basal immunity against PPV, ii) Functional characterization of PPV effectors suppressing plant basal immunity, and iii) Evaluation of the overlap between the basal immunity pathways triggered by plant pathogens.
In order to determine whether the proteins already identified in plant basal immunity against non-viral pathogens could play also a role in plant resistance to viruses, Arabidopsis reverse genetics analyses have been performed. The results revealed the role of the PTI machinery in Arabidopsis resistance to PPV, strengthening the double hypothesis that plants defend themselves against viruses through basal immunity and that basal immunity pathways against viral pathogens are at least partially shared with basal immunity pathways against non-viral pathogens. In addition, one PPV protein negatively regulates PAMP-triggered responses, revealing for the first time that the genome of plant viruses encode PTI suppressing-pathogenic effectors.
PERSPECTIVE: HOW CAN SCIENCE TRANSLATE PTI-MEDIATED ANTIVIRAL MECHANISMS TOWARDS CROP IMPROVEMENT?
So far, the only powerful strategy to control viral epidemics in field relies on the use of genetic resistances. Crop improvement programs aim at obtaining new resistant varieties, blocking viral multiplication and/or limiting virus-associated damages. Unfortunately, by their inherent nature, viruses evolve very quickly the ability to overcome the resistances employed by breeders. Hence, the extreme genetic plasticity of viruses represents a major challenge for the coming years. The efficiency and durability of resistance mechanisms depend mostly upon the resistance timing of action and the conservation of the pathogen elicitor molecule into the pathogen family. In this context, PTI mechanisms will combine these criteria, as PTI-associated defense reactions are extremely fast and antiviral PTI is triggered by viral nucleic acids (well characterized in the animal field) highly characteristic of viruses. Therefore, translating fundamental knowledge about antiviral PTI mechanisms into crop improvement programs will bring considerable advances in the control of viral epidemics in fields.