A trimeric CrRLK1L-LLG1 complex genetically modulates SUMM2-mediated autoimmunity

Yanyan Huang, Chuanchun Yin, Jun Liu, Baomin Feng, Dongdong Ge, Liang Kong, Fausto Andres Ortiz-Morea, Julia Richter, Marie-Theres Hauser, Wen-Ming Wang, Libo Shan and Ping He ()
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Yanyan Huang: State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China, Sichuan Agricultural University
Chuanchun Yin: State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China, Sichuan Agricultural University
Jun Liu: Institute for Plant Genomics & Biotechnology, Texas A&M University
Baomin Feng: Institute for Plant Genomics & Biotechnology, Texas A&M University
Dongdong Ge: Institute for Plant Genomics & Biotechnology, Texas A&M University
Liang Kong: Institute for Plant Genomics & Biotechnology, Texas A&M University
Fausto Andres Ortiz-Morea: Institute for Plant Genomics & Biotechnology, Texas A&M University
Julia Richter: University of Natural Resources and Life Sciences, Vienna (BOKU)
Marie-Theres Hauser: University of Natural Resources and Life Sciences, Vienna (BOKU)
Wen-Ming Wang: State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China, Sichuan Agricultural University
Libo Shan: Institute for Plant Genomics & Biotechnology, Texas A&M University
Ping He: Institute for Plant Genomics & Biotechnology, Texas A&M University

Nature Communications, 2020, vol. 11, issue 1, 1-15

Abstract: Abstract Cell death is intrinsically linked with immunity. Disruption of an immune-activated MAPK cascade, consisting of MEKK1, MKK1/2, and MPK4, triggers cell death and autoimmunity through the nucleotide-binding leucine-rich repeat (NLR) protein SUMM2 and the MAPK kinase kinase MEKK2. In this study, we identify a Catharanthus roseus receptor-like kinase 1-like (CrRLK1L), named LETUM2/MEDOS1 (LET2/MDS1), and the glycosylphosphatidylinositol (GPI)-anchored protein LLG1 as regulators of mekk1-mkk1/2-mpk4 cell death. LET2/MDS1 functions additively with LET1, another CrRLK1L, and acts genetically downstream of MEKK2 in regulating SUMM2 activation. LET2/MDS1 complexes with LET1 and promotes LET1 phosphorylation, revealing an intertwined regulation between different CrRLK1Ls. LLG1 interacts with the ectodomain of LET1/2 and mediates LET1/2 transport to the plasma membrane, corroborating its function as a co-receptor of LET1/2 in the mekk1-mkk1/2-mpk4 cell death pathway. Thus, our data suggest that a trimeric complex consisting of two CrRLK1Ls LET1, LET2/MDS1, and a GPI-anchored protein LLG1 that regulates the activation of NLR SUMM2 for initiating cell death and autoimmunity.

Date: 2020
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DOI: 10.1038/s41467-020-18600-8

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