Plants can perceive attacking pathogens via the recognition of conserved Pathogen Associated Molecular Patterns (PAMPs) resulting in activation of a multi-level plant defence. Pathogens have evolved mechanisms to attenuate PAMP-triggered immunity (PTI) via specialized “effector” proteins translocated to the host cell. Effectors can influence diverse host cell pathways in order to manipulate the cell metabolism for the benefit of the pathogen. However, plants have involved specific resistance (R) proteins for pathogen effector recognition, which initiates strong defence culminating in a localized hypersensitive cell death response (HR), restricting pathogen spread (Effector Triggered Immunity, or ETI). Although PTI and ETI result in similar responses, the links between PTI and ETI remain obscure. The study of R protein recognition and signaling requires a well-established model system. The Arabidopsis thaliana resistance genes RRS1 and RPS4, encode TIR-NB-LRR proteins which confer resistance to baterial pathogens carrying the effector genes popP2 and avrRps4 respectively.
The overall aim of this proposal is to enhance our understanding of defence activation during ETI, and possible overlaps with PTI, by understanding the mechanisms of R-effector recognition and how this signals various defence responses. The work is strategically relevant as it aims to underpin the delivery of sustainable immunity in important crop species.
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