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

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  • Yanyan Huang

    (State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China, Sichuan Agricultural University
    Institute for Plant Genomics & Biotechnology, Texas A&M University)

  • Chuanchun Yin

    (State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China, Sichuan Agricultural University
    Institute for Plant Genomics & Biotechnology, Texas A&M University)

  • Jun Liu

    (Institute for Plant Genomics & Biotechnology, Texas A&M University)

  • Baomin Feng

    (Institute for Plant Genomics & Biotechnology, Texas A&M University
    State Key Laboratory of Ecological Control of Fujian-Taiwan Crop Pests, Key Laboratory of Ministry of Education for Genetics, Breeding and Multiple Utilization of Crops, Plant Immunity Center, Fujian Agriculture and Forestry 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)

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.

Suggested Citation

  • 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 & Ping He, 2020. "A trimeric CrRLK1L-LLG1 complex genetically modulates SUMM2-mediated autoimmunity," Nature Communications, Nature, vol. 11(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-18600-8
    DOI: 10.1038/s41467-020-18600-8
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    Cited by:

    1. Ronny Völz & William Harris & Heribert Hirt & Yong-Hwan Lee, 2022. "ROS homeostasis mediated by MPK4 and SUMM2 determines synergid cell death," Nature Communications, Nature, vol. 13(1), pages 1-12, December.

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