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BIO2012-35641: Suppression of effector-triggered immunity and its role on the adaptation of Pseudomonas syringae to the host

Dates: from 1/1/2013 to 31/12/2015
Funding: Plan Nacional, MINECO. Co-financiado por fondos FEDER.
Participants: UMA
Principal Investigator: Carmen R. Beuzón López
Researchers: Carmen R. Beuzón López, Ainhoa Lucia Quintana, Javier Ruiz Albert, Rosas Diaz, Tábata.
Link: http://

Plant inmunity against bacterial pathogens can be classified into two categories according to the type of molecule detected: immunity triggered by microbe-associated molecular patterns (MTI), which can be suppressed by bacterial efectors, and effector-triggered immunity (ETI), which can also be suppressed by effectors, and is considered the most efficient and robust line of defence against well-adapted pathogens. Although a number of effectors have been shown to suppress ETI, this activity has been demonstrated following overexpression of individual effectors in heterologous systems, o directly into the plant. Therefore, the relevance of these activities in their natural pathosystems and their contribution to host adaptacion is yet to be established. Results obtained in our current project show that establishing the biological relevance of effector function during the infection process should include its analysis within the context of the pathogen that encodes it, together with the rest of the effectors from that pathogen, and on the relevant pathosystem, in order to allow detection of functional relationships between effectors and their relevance to host adaptation. In the Pph 1448a-bean model, we have demonstrated that functional interaction between effectors from the same pathogen is not an occasional event, but rather frequent and that can reach a considerable complexity. We have found a clear example in the interaction of another pathovar of P. syringae with bean, with the HopZ effector family, where we have demonstrated that the ETI triggered by these effectors can be efficiently suppressed by another effector from the same pathogen, thus determining avoidance of plant resistance. The analysis of functional relationshsips between effectors also led us to identify the capability of one effector of the HopZ family to suppress ETI and SAR responses triggered through different signalling cascades, impliying that the mecanism of suppression involved is general and novel. These results indicate that, as a consecuence of the individual study of effectors isolated from its natural pathosystem, routinely used in the field, the importance of the functional relationships between effectors has been underestimated. Our working hypothesis is that detailed analysis of these relationships, with a particular attention to crossed suppression of ETI between effectors from the same pathogen, will provide relevant information about the mechanisms of evolution and host adaptation in P. syringae, potentially crucial for the design and selección of efficient and durable crop protection estrategies against this pathogen. For that purpose, we plan to extend the knowledge acquired in the virulence function of Pph 1448a effectors within bean, characterizing such functions and their relationships through the analysis of their combined expression in bean. Furthermore, with the same purpose of characterizing functional relationships between effectors from another pathovar of P. syringae also adapted to bean, we will aim to identify the effector responsible for suppressing the HopZ1a-triggered ETI in bean. Considering the elevated interest that identifying new virulence targets have in the process of designing crop protection estrategies, we have included as an additional aim the molecular characterization of the ETI/ SAR supression mechanism of HopZ1a, taking full advantage of the results, tools and experimental approaches previously generated by our team.

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