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Calcium-regulated signalling network meets atypical NLR immune receptor: Control of CPK5-dependent plant defence initiation and immune signal propagation through TN2 and EXO70B1

Subject Area Organismic Interactions, Chemical Ecology and Microbiomes of Plant Systems
Plant Biochemistry and Biophysics
Term from 2018 to 2023
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 391652390
 
Final Report Year 2023

Final Report Abstract

Pathogens target key signalling hubs to subvert plant immune systems, one of which is EXO70B1, an exocyst subunit needed for vesicle anchoring and tethering to the plasma membrane during exocytosis. Pathogen-induced disappearance of EXO70B1 (or its absence in an exo70B1 null mutant) trigger (auto)immunity responses that are dependent on the atypical NLR protein TN2, as well as the calcium-dependent protein kinase 5 (CPK5). The results of this Sino-German collaborative study suggest that TN2 acts as a guard monitoring the integrity of EXO70B1, while CPK5 is a key executor of this immunity pathway by activating downstream components. This explains why overexpressing CPK5 can phenocopy the exo70B1 mutant, resulting in TN2-dependent autoimmunity and enhanced disease resistance. Mechanistically, upon release from a EXO70B1-TN2 complex, TN2 binds activated CPK5 to enable sustained kinase activity that no longer requires calcium-induced re-activation, thus leading to CPK5-dependent signal propagation, amplification and long-term systemic immune signalling. Since TN2 signalling subsequently engages so-called ADR1 helper NLRs that can assemble into calcium-permeable pores, feed-forward loops into calcium-based, and most likely CPK5-based, immune signalling may be anticipated. The findings of this and ongoing studies will advance the understanding of key EXO70B1 functions and immune regulators such as TN2 and CPK5, so that strategies to protect important crops from infection may be developed in the future.

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