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

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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.