Coordination of plant immunity and abiotic stress by CEP peptides

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Pathogens pose a significant problem for agriculture and food security. Plants also face abiotic stresses that impede crop productivity. Receptor kinases (RKs) are key components of plant immunity by perceiving exogenous danger molecules. RKs also sense endogenous peptides to control plant growth and development and several of these fine-tune plant immune responses. Immune-modulatory peptides were classified as phytocytokines and also regulate abiotic stress responses, but the underlying mechanisms remain largely unknown. The project builds on the identification of C-TERMINALLY ENCODED PEPTIDES (CEPs) as phytocytokines in Arabidopsis, which were previously shown to regulate root growth and responses to nitrogen (N) starvation. We demonstrated that some group I CEPs are inducers of immune responses and required for resistance to bacterial pathogens. They are perceived by three tissue-specific receptors, CEP RECEPTOR 1 (CEPR1), CEPR2 and the related RECEPTOR-LIKE KINASE 7 with distinct specificities for different CEPs. Our work revealed that N limitation promotes CEP-dependent immunity, suggesting that CEPs coordinate a cross-talk between immunity and N sensing. Our preliminary data suggests that different CEP ligands employ specific co-receptors and downstream components for signalling. CEP receptors interact with pattern recognition receptors (PRRs) and CEPs promote N status-dependent PRR abundance. Finally, we noticed that group II CEPs are novel phytocytokines with distinct receptor and co-receptor dependency. Based on my preliminary work, I raise three main hypotheses that underscore this research proposal: (1) CEPs induce tissue-specific responses via distinct receptor complexes; (2) CEP and CEP receptors directly promote cell surface immunity under N limitation by modulating FLS2 accumulation and signaling; (3) Class II CEPs are a novel family of phytocytokines that are specifically perceived in stomata to integrate biotic and abiotic stress. We will challenge these hypotheses by dissecting ligand-specific mechanisms of CEP receptor complex formation and tissue-specificity of CEP signalling. We will decipher the mechanistic basis of CEP-mediated control of cell surface immunity upon N limitation and elucidate the biological role and perception mechanism of class II CEPs, a yet undescribed (sub)family of phytocytokines. The expected findings will provide important insights into specificity of phytocytokine signaling. Moreover, deciphering the mechanistic basis of N and CEP-dependent modulation of immunity may generate transferable knowledge for future crop improvement strategies.