Serveur d'exploration sur les récepteurs immunitaires végétaux

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The malectin-like receptor-like kinase LETUM1 modulates NLR protein SUMM2 activation via MEKK2 scaffolding.

Identifieur interne : 000021 ( Main/Exploration ); précédent : 000020; suivant : 000022

The malectin-like receptor-like kinase LETUM1 modulates NLR protein SUMM2 activation via MEKK2 scaffolding.

Auteurs : Jun Liu [États-Unis] ; Yanyan Huang [États-Unis, République populaire de Chine] ; Liang Kong [États-Unis] ; Xiao Yu [États-Unis] ; Baomin Feng [États-Unis] ; Derui Liu [États-Unis] ; Baoyu Zhao [États-Unis] ; Giselle C. Mendes [États-Unis, Brésil] ; Peiguo Yuan [États-Unis] ; Dongdong Ge [États-Unis] ; Wen-Ming Wang [République populaire de Chine] ; Elizabeth P B. Fontes [Brésil] ; Pingwei Li [États-Unis] ; Libo Shan [États-Unis] ; Ping He [États-Unis]

Source :

RBID : pubmed:32839517

Abstract

The innate immune system detects pathogen-derived molecules via specialized immune receptors to prevent infections1-3. 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 autoimmunity4-9. To gain insights into the mechanisms underlying SUMM2 activation, we used an RNA interference-based genetic screen for mekk1 autoimmune suppressors and identified an uncharacterized malectin-like RLK, named LETUM1 (LET1), as a specific regulator of mekk1-mkk1/2-mpk4 autoimmunity 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.

DOI: 10.1038/s41477-020-0748-6
PubMed: 32839517
PubMed Central: PMC7492416


Affiliations:


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<name sortKey="Ge, Dongdong" sort="Ge, Dongdong" uniqKey="Ge D" first="Dongdong" last="Ge">Dongdong Ge</name>
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<name sortKey="Li, Pingwei" sort="Li, Pingwei" uniqKey="Li P" first="Pingwei" last="Li">Pingwei Li</name>
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<name sortKey="Kong, Liang" sort="Kong, Liang" uniqKey="Kong L" first="Liang" last="Kong">Liang Kong</name>
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<name sortKey="Yu, Xiao" sort="Yu, Xiao" uniqKey="Yu X" first="Xiao" last="Yu">Xiao Yu</name>
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<name sortKey="Feng, Baomin" sort="Feng, Baomin" uniqKey="Feng B" first="Baomin" last="Feng">Baomin Feng</name>
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<name sortKey="Liu, Derui" sort="Liu, Derui" uniqKey="Liu D" first="Derui" last="Liu">Derui Liu</name>
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<name sortKey="Zhao, Baoyu" sort="Zhao, Baoyu" uniqKey="Zhao B" first="Baoyu" last="Zhao">Baoyu Zhao</name>
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<nlm:affiliation>Department of Biochemistry & Biophysics, Texas A&M University, College Station, TX, USA.</nlm:affiliation>
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<name sortKey="Mendes, Giselle C" sort="Mendes, Giselle C" uniqKey="Mendes G" first="Giselle C" last="Mendes">Giselle C. Mendes</name>
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<name sortKey="Li, Pingwei" sort="Li, Pingwei" uniqKey="Li P" first="Pingwei" last="Li">Pingwei Li</name>
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<title level="j">Nature plants</title>
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<div type="abstract" xml:lang="en">The innate immune system detects pathogen-derived molecules via specialized immune receptors to prevent infections
<sup>1-3</sup>
. 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
<sup>4-9</sup>
. To gain insights into the mechanisms underlying SUMM2 activation, we used an RNA interference-based genetic screen for mekk1 autoimmune suppressors and identified an uncharacterized malectin-like RLK, named LETUM1 (LET1), as a specific regulator of mekk1-mkk1/2-mpk4 autoimmunity 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.</div>
</front>
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<Month>11</Month>
<Day>10</Day>
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<Volume>6</Volume>
<Issue>9</Issue>
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<Month>09</Month>
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<Title>Nature plants</Title>
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<ArticleTitle>The malectin-like receptor-like kinase LETUM1 modulates NLR protein SUMM2 activation via MEKK2 scaffolding.</ArticleTitle>
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<Abstract>
<AbstractText>The innate immune system detects pathogen-derived molecules via specialized immune receptors to prevent infections
<sup>1-3</sup>
. 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
<sup>4-9</sup>
. To gain insights into the mechanisms underlying SUMM2 activation, we used an RNA interference-based genetic screen for mekk1 autoimmune suppressors and identified an uncharacterized malectin-like RLK, named LETUM1 (LET1), as a specific regulator of mekk1-mkk1/2-mpk4 autoimmunity 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.</AbstractText>
</Abstract>
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<ForeName>Jun</ForeName>
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<Affiliation>Institute for Plant Genomics & Biotechnology, Texas A&M University, College Station, TX, USA.</Affiliation>
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<LastName>Kong</LastName>
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<AffiliationInfo>
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<LastName>Zhao</LastName>
<ForeName>Baoyu</ForeName>
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<ForeName>Giselle C</ForeName>
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</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Department of Biochemistry & Biophysics, Texas A&M University, College Station, TX, USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>National Institute of Science and Technology in Plant-Pest Interactions and Department of Biochemistry and Molecular Biology, Universidade Federal de Viçosa, Viçosa, Brazil.</Affiliation>
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<Author ValidYN="Y">
<LastName>Yuan</LastName>
<ForeName>Peiguo</ForeName>
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<Affiliation>National Institute of Science and Technology in Plant-Pest Interactions and Department of Biochemistry and Molecular Biology, Universidade Federal de Viçosa, Viçosa, Brazil.</Affiliation>
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<LastName>Shan</LastName>
<ForeName>Libo</ForeName>
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<Affiliation>Institute for Plant Genomics & Biotechnology, Texas A&M University, College Station, TX, USA. pinghe@tamu.edu.</Affiliation>
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