Coordination of plant immunity and abiotic stress by CEP peptides

CEP 肽协调植物免疫和非生物胁迫

• 批准号: 450044414
• 负责人: Dr. Martin Stegmann
• 金额: --
• 依托单位: Lehrstuhl für Phytopathologie
• 依托单位国家: 德国
• 项目类别: Research Grants
• 资助国家: 德国
• 项目状态: 未结题
• 来源: https://gepris.dfg.de/gepris/projekt/450044414?language=en
• 关键词: Coordination; plant; immunity; abiotic; stress

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.

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胁迫。受体激酶（Receptor Kinases，RKs）是植物免疫的关键组分，通过感知外源危险分子而发挥作用. RKs还感测内源性肽以控制植物生长和发育，并且这些中的一些微调植物免疫应答。免疫调节肽被归类为植物细胞因子，也可调节非生物胁迫反应，但其潜在机制仍不清楚。该项目建立在C-乙酰基编码肽（CEP）作为拟南芥中的植物细胞因子的鉴定的基础上，这些细胞因子先前被证明可以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是免疫应答的诱导剂，并且是抵抗细菌病原体所必需的。它们被三种组织特异性受体感知，即CEP受体1（CEPR 1）、CEPR 2和相关的受体样激酶7，对不同的CEP具有不同的特异性。我们的工作表明，N限制促进CEP依赖性免疫，这表明CEP协调免疫和N传感之间的串扰。我们的初步数据表明，不同的CEP配体采用特定的共受体和下游组件的信号。CEP受体与模式识别受体（PRR）相互作用，CEP促进N状态依赖性PRR丰度。最后，我们注意到II组CEP是具有不同受体和共受体依赖性的新型植物细胞因子。基于我的前期工作，我提出了三个主要假设：（1）CEP通过不同的受体复合物诱导组织特异性反应;（2）CEP和CEP受体通过调节FLS 2的积累和信号传导直接促进N限制下的细胞表面免疫;（3）II类CEPs是一类新的植物细胞因子家族，它们在气孔中特异性地被感知以整合生物和非生物胁迫。我们将挑战这些假设解剖配体特异性机制的CEP受体复合物的形成和组织特异性的CEP信号。我们将破译CEP介导的控制细胞表面免疫N限制的机制基础，并阐明生物学作用和感知机制的II类CEP，尚未描述的（子）家族的植物细胞因子。预期的研究结果将提供重要的见解特异性的植物细胞因子信号。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。