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UBC Theses and Dissertations

The roles of MUSE1 and MUSE15 in plant innate immunity Dong, Xiaoou

Abstract

Nucleotide-binding leucine-rich repeat (NLR) immune receptors play crucial roles in pathogen recognition and defense activation in animals and plants. The immune responses mediated by NLR proteins are tightly regulated in plants so that the host effectively responds to pathogen attack without experiencing autoimmunity. However, the mechanisms underlying this regulation are not fully understood. To better understand this process, a mutant snc1-enhancing (MUSE) forward genetic screen was performed in model plant Arabidopsis thaliana. This thesis describes the identification and characterization of two genes encoding negative regulators of defense responses, MUSE1 and MUSE15, respectively. MUSE1 encodes a previously uncharacterized RING domain protein exhibiting E3 ubiquitin ligase activity. It has a close paralog in the Arabidopsis genome, which is MUSE2. Albeit both muse1 and muse2 single mutants are wild type (WT)-like, the muse1 muse2 double knockout mutant displays severe autoimmunity, suggesting their overlapping functions in regulating defense. Through epistatic analysis, it was found that the autoimmunity of muse1 muse2 is fully dependent on SNC1, suggesting that MUSE1 and MUSE2 are specifically involved in the regulation of SNC1-mediated immunity. Genetic and biochemical analyses excluded SNC1, bHLH84 and MOS10 from being potential ubiquitination substrates of MUSE1 and MUSE2, and offered clues to the identity of the substrates of MUSE1 and MUSE2. These findings add to the growing list of characterized E3 ubiquitin ligases involved in the stringent regulation of NLR-mediated immunity. MUSE15 encodes ADR1-L1, which belongs to the ADR1 helper NLR family. Previous studies have demonstrated that the ADR1 family is required for defense mediated by multiple sensor NLRs. Unexpectedly, loss of ADR1-L1 enhances immunity-related phenotypes in multiple autoimmune mutants including snc1, cpr1, bal and lsd1. This immunity-enhancing effect is not mediated by increased SNC1 protein stability, nor is it fully dependent on the accumulation of defense hormone salicylic acid (SA). Transcriptional analysis revealed an up-regulation of ADR1 and ADR1-L2 in the adr1-L1 background, which may over-compensate the loss of ADR1-L1, leading to stronger defense responses. The complex regulation within the ADR1 family extends our knowledge on the interplay among helper NLRs.

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