期刊
NATURE PLANTS
卷 6, 期 9, 页码 1106-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41477-020-0748-6
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资金
- National Institutes of Health (NIH) [R01GM092893]
- National Science Foundation (NSF) [MCB-1906060]
- NIH [R01GM097247]
- Robert A. Welch Foundation [A-1795]
- China Scholarship Council (CSC)
- INCT/CNPq Fellowship, Brazil
The innate immune system detects pathogen-derived molecules via specialized immune receptors to prevent infections(1-3). Plant immune receptors include cell surface-resident pattern recognition receptors (PRRs, including receptor-like kinases (RLKs)), and intracellular nucleotide-binding domain leucine-rich repeat proteins (NLRs). It remains enigmatic how RLK- and NLR-mediated signalling are connected. Disruption of an immune-activated MEKK1-MKK1/2-MPK4 MAPK cascade activates the NLR SUMM2 via the MAPK kinase kinase MEKK2, leading to autoimmunity(4-9). To gain insights into the mechanisms underlying SUMM2 activation, we used an RNA interference-based genetic screen formekk1autoimmune suppressors and identified an uncharacterized malectin-like RLK, named LETUM1 (LET1), as a specific regulator ofmekk1-mkk1/2-mpk4autoimmunity via complexing with both SUMM2 and MEKK2. MEKK2 scaffolds LET1 and SUMM2 for protein stability and association, and counter-regulates the F-box protein CPR1-mediated SUMM2 ubiquitination and degradation, thereby regulating SUMM2 accumulation and activation. Our study indicates that malectin-like RLK LET1 senses the perturbance of cellular homoeostasis caused by the deficiency in immune-activated signalling and activates the NLR SUMM2-mediated autoimmunity via MEKK2 scaffolding. Plants with loss of function mutations in the MEKK1-MKK1/2-MPK4 MAP kinase pathway show strong autoimmunity phenotypes and dwarfism. Through a suppressor genetic screen, the malectin-like receptor kinase LET1 is identified as a new regulator of immune signalling.
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