Non-coding RNA based regulation of the LRR-RLKs mediated immunity

作为持续受到一系列恶劣环境因素威胁的固着生物，植物的基因组编码了几个细胞表面受体家族，包括扩展的富含亮氨酸重复序列的受体样激酶(LRR-RLKs)。这些受体感知有关多种环境因素的信息，包括生长条件和病原体的存在，并将它们整合在一起，以确保最佳适应性。负责病原体感知的LRR-RLK的子集称为模式识别受体(PRRs)。它们通过识别被称为微生物相关分子模式(MAMPs)的入侵者在进化上保守的分子特征，形成抵御微生物攻击的第一道防线。识别启动一种名为模式触发免疫(PTI)的强大先天免疫反应，以限制病原体的生长。为了最大化植物的适应性，防御相关基因必须通过转录、转录后和翻译后机制进行严格调控，以避免在没有病原体的情况下代价高昂的免疫系统激活，同时确保对病原菌的攻击做出及时的防御反应。非编码RNA(NcRNAs)是通过转录和转录后机制调节基因表达的关键分子。根据序列长度，它们可以分为小RNA(SRNAs)和长非编码RNAs(LncRNAs)。这项建议的目的是确定ncRNAs调节LRR-RLKs介导的免疫反应的机制。拟议中的调查沿着两条独立的路线进行。在第一部分中，我将展示LRR-RLKs在调节免疫攻击时ncRNAs的生物发生中的核心作用。在第二部分中，我将研究LRR-RLK本身是如何被这些ncRNAs调控的，以便微调植物的免疫反应。这两个独立的实验研究将加深我们对植物免疫系统是如何通过LRR-RLKs下游信号网络之间复杂的相互作用来调节的理解。

Being sessile organisms that are continuously threatened by a range of hostile environmental factors, plants have genomes that encode several families of cell surface receptors, including the expanded Leucine-Rich Repeat Receptor-Like Kinases (LRR-RLKs). These receptors perceive information about multiple environmental factors, including growth conditions and pathogen presence, and integrate them to ensure optimal fitness. The subset of LRR-RLKs responsible for pathogen perception are termed Pattern Recognition Receptors (PRRs). They form the first line of defense against microbial attack by recognizing evolutionarily conserved molecular signatures of invaders called Microbe Associated Molecular Patterns (MAMPs). Recognition initiates a robust innate immune response called Pattern-Triggered Immunity (PTI) to limit pathogen growth. To maximize plant fitness, defense-related genes must be tightly regulated through transcriptional, post-transcriptional, and post-translational mechanisms to avoid costly immune system activation in the absence of pathogens, while ensuring timely defense response upon pathogen challenge. Non-coding RNAs (ncRNAs) are key regulators of gene expression through transcriptional and post-transcriptional mechanisms. They can be classified as either small RNAs (sRNAs) or long-non-coding RNAs (lncRNAs) based on sequence length. The goal of this proposal is to determine the mechanisms by which ncRNAs regulate the immune responses mediated by LRR-RLKs. The proposed investigations run along two independent lines. In the first part, I will demonstrate the central role of LRR-RLKs in regulating the biogenesis of ncRNAs upon immune challenge. In the second part, I will investigate how LRR-RLKs are themselves regulated by these ncRNAs in order to fine-tune the plant immune response. These two independent experimental investigations will deepen our understanding of how the plant immune system is regulated through the intricate interplay between signaling networks downstream of the LRR-RLKs.