Dissection of CEP signalling specificity coordinating plant nitrogen status with immunity

• Applicant: Professor Dr. Martin Stegmann
• Subject Area: Plant Physiology ; Organismic Interactions, Chemical Ecology and Microbiomes of Plant Systems ; Plant Breeding and Plant Pathology
• Term: since 2020
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 450044414

Pathogens pose a significant problem for agriculture and food security. Plants also face abiotic stresses that impede crop productivity, including fluctuating nutrient availabilities. 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 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 (RLK7) with distinct specificities for different CEPs. Our work revealed that the plants N status regulates CEP-dependent immunity, suggesting that CEPs coordinate a cross-talk between immunity and N sensing. Our preliminary data further suggest that different CEP ligands show distinct receptor requirements and employ specific co-receptors for signalling. CEP receptors interact with pattern recognition receptors (PRRs) and CEPs promote N status-dependent PRR abundance. Based on my preliminary work, I raise four main hypotheses that underscore this research proposal: (1) CEPs induce tissue-specific responses via distinct receptor; (2) CEPRs and RLK7 show distinct ligand and co-receptor specificities; (3) CEP and their receptors directly promote FLS2 signalling and cell surface immunity; (4) CEPs coordinate the plants N status with cell surface immunity. We will challenge these hypotheses by dissecting tissue-specificity of CEP signalling and ligand-specific mechanisms of CEP receptor complex formation. We will decipher the mechanistic basis and extent of CEP-mediated control of cell surface immunity and further explore the molecular basis of CEP-dependent cross-talk between N homeostasis and immunity. The expected findings will provide important insights into specificity of phytocytokine signalling. Moreover, deciphering the mechanistic basis of N and CEP-dependent modulation of immunity may generate transferable knowledge for future crop improvement strategies.

• DFG Programme: Research Grants