Coordination of plant immunity and abiotic stress by CEP peptides

病原体对农业和粮食安全构成重大问题。植物还面临着阻碍作物生产力的非生物压力。受体激酶(RKS)是植物免疫的重要组成部分，通过感知外源危险分子而发挥作用。RKS还感应内源性多肽来控制植物的生长和发育，以及其中几种微调的植物免疫反应。免疫调节肽被归类为植物细胞因子，也调节非生物应激反应，但其潜在机制仍很大程度上尚不清楚。该项目的基础是确定C末端编码肽(CEP)是拟南芥中的植物细胞因子，以前被证明调节根的生长和对氮(N)饥饿的反应。我们证明了一些I组CEP是免疫反应的诱导者，是抵抗细菌病原体所必需的。它们被CEP受体1(CEPR1)、CEPR2和相关的受体样激酶7三种组织特异性受体所感知，对不同的CEP具有不同的特异性。我们的工作揭示了N限制促进CEP依赖的免疫，这表明CEP协调免疫和N感觉之间的串扰。我们的初步数据表明，不同的CEP配体使用特定的辅助受体和下游成分进行信号传递。CEP受体与模式识别受体(PRRs)相互作用，CEP促进N状态依赖的PRR丰度。最后，我们注意到第二组CEPS是一种新的植物细胞因子，具有明显的受体和共受体依赖性。在我前期工作的基础上，我提出了三个主要假设来支持这项研究：(1)CEP通过不同的受体复合体诱导组织特异性反应；(2)CEP和CEP受体通过调节Fls2的积累和信号转导，直接促进N限制下的细胞表面免疫；(3)第二类CEP是一个新的植物细胞因子家族，专门在气孔中识别，整合生物和非生物胁迫。我们将通过剖析CEP受体复合体形成的配体特异性机制和CEP信号的组织特异性来挑战这些假说。我们将破译CEP介导的细胞表面免疫对N限制的机制基础，并阐明II类CEPs的生物学作用和感知机制，这是一个尚未描述的(亚)植物细胞因子家族。这些预期的发现将为了解植物细胞因子信号的特异性提供重要的见解。此外，破译N和CEP依赖的免疫调节的机制基础可能会为未来的作物改良策略产生可转移的知识。

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.