PlantImRecepV1, Main, Exploration, bibRecord, 000221

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

Identifieur interne : 000221 ( Main/Exploration ); précédent : 000220; suivant : 000222

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

Auteurs : Yanyan Huang [République populaire de Chine, États-Unis] ; Chuanchun Yin [République populaire de Chine, États-Unis] ; Jun Liu [États-Unis] ; Baomin Feng [États-Unis, République populaire de Chine] ; Dongdong Ge [États-Unis] ; Liang Kong [États-Unis] ; Fausto Andres Ortiz-Morea [États-Unis] ; Julia Richter [Autriche] ; Marie-Theres Hauser [Autriche] ; Wen-Ming Wang [République populaire de Chine] ; Libo Shan [États-Unis] ; Ping He [États-Unis]

Source :

Nature communications [ 2041-1723 ] ; 2020.

RBID : pubmed:32978401

Descripteurs français

English descriptors

KwdEn :
- Arabidopsis (genetics), Arabidopsis (metabolism), Arabidopsis Proteins (genetics), Arabidopsis Proteins (metabolism), Autoimmunity (genetics), Autoimmunity (physiology), Carrier Proteins (genetics), Carrier Proteins (immunology), Carrier Proteins (metabolism), Catharanthus (genetics), Catharanthus (metabolism), Cell Death (genetics), GPI-Linked Proteins (genetics), GPI-Linked Proteins (metabolism), Gene Expression Regulation, Plant (MeSH), Glycosylphosphatidylinositols (MeSH), MAP Kinase Kinase Kinases (genetics), MAP Kinase Signaling System (MeSH), Mitogen-Activated Protein Kinase Kinases (metabolism), Phosphorylation (MeSH), Plant Proteins (genetics), Plant Proteins (immunology), Plant Proteins (metabolism), Plants, Genetically Modified (MeSH), RNA Interference (MeSH), Transcriptome (MeSH).
MESH :
- chemical , genetics : Arabidopsis Proteins, Carrier Proteins, GPI-Linked Proteins, MAP Kinase Kinase Kinases, Plant Proteins.
- genetics : Arabidopsis, Autoimmunity, Catharanthus, Cell Death.
- chemical , immunology : Carrier Proteins, Plant Proteins.
- metabolism : Arabidopsis, Arabidopsis Proteins, Carrier Proteins, Catharanthus, GPI-Linked Proteins, Mitogen-Activated Protein Kinase Kinases, Plant Proteins.
- physiology : Autoimmunity.
- Gene Expression Regulation, Plant, Glycosylphosphatidylinositols, MAP Kinase Signaling System, Phosphorylation, Plants, Genetically Modified, RNA Interference, Transcriptome.

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.

DOI: 10.1038/s41467-020-18600-8
PubMed: 32978401
PubMed Central: PMC7519094

Affiliations:

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Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Arabidopsis (genetics)</term>
<term>Arabidopsis (metabolism)</term>
<term>Arabidopsis Proteins (genetics)</term>
<term>Arabidopsis Proteins (metabolism)</term>
<term>Autoimmunity (genetics)</term>
<term>Autoimmunity (physiology)</term>
<term>Carrier Proteins (genetics)</term>
<term>Carrier Proteins (immunology)</term>
<term>Carrier Proteins (metabolism)</term>
<term>Catharanthus (genetics)</term>
<term>Catharanthus (metabolism)</term>
<term>Cell Death (genetics)</term>
<term>GPI-Linked Proteins (genetics)</term>
<term>GPI-Linked Proteins (metabolism)</term>
<term>Gene Expression Regulation, Plant (MeSH)</term>
<term>Glycosylphosphatidylinositols (MeSH)</term>
<term>MAP Kinase Kinase Kinases (genetics)</term>
<term>MAP Kinase Signaling System (MeSH)</term>
<term>Mitogen-Activated Protein Kinase Kinases (metabolism)</term>
<term>Phosphorylation (MeSH)</term>
<term>Plant Proteins (genetics)</term>
<term>Plant Proteins (immunology)</term>
<term>Plant Proteins (metabolism)</term>
<term>Plants, Genetically Modified (MeSH)</term>
<term>RNA Interference (MeSH)</term>
<term>Transcriptome (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Arabidopsis (génétique)</term>
<term>Arabidopsis (métabolisme)</term>
<term>Auto-immunité (génétique)</term>
<term>Auto-immunité (physiologie)</term>
<term>Catharanthus (génétique)</term>
<term>Catharanthus (métabolisme)</term>
<term>Glycosylphosphatidylinositols (MeSH)</term>
<term>Interférence par ARN (MeSH)</term>
<term>MAP Kinase Kinase Kinases (génétique)</term>
<term>Mitogen-Activated Protein Kinase Kinases (métabolisme)</term>
<term>Mort cellulaire (génétique)</term>
<term>Phosphorylation (MeSH)</term>
<term>Protéines d'Arabidopsis (génétique)</term>
<term>Protéines d'Arabidopsis (métabolisme)</term>
<term>Protéines de transport (génétique)</term>
<term>Protéines de transport (immunologie)</term>
<term>Protéines de transport (métabolisme)</term>
<term>Protéines liées au GPI (génétique)</term>
<term>Protéines liées au GPI (métabolisme)</term>
<term>Protéines végétales (génétique)</term>
<term>Protéines végétales (immunologie)</term>
<term>Protéines végétales (métabolisme)</term>
<term>Régulation de l'expression des gènes végétaux (MeSH)</term>
<term>Système de signalisation des MAP kinases (MeSH)</term>
<term>Transcriptome (MeSH)</term>
<term>Végétaux génétiquement modifiés (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Arabidopsis Proteins</term>
<term>Carrier Proteins</term>
<term>GPI-Linked Proteins</term>
<term>MAP Kinase Kinase Kinases</term>
<term>Plant Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Arabidopsis</term>
<term>Autoimmunity</term>
<term>Catharanthus</term>
<term>Cell Death</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Arabidopsis</term>
<term>Auto-immunité</term>
<term>Catharanthus</term>
<term>MAP Kinase Kinase Kinases</term>
<term>Mort cellulaire</term>
<term>Protéines d'Arabidopsis</term>
<term>Protéines de transport</term>
<term>Protéines liées au GPI</term>
<term>Protéines végétales</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Protéines de transport</term>
<term>Protéines végétales</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Carrier Proteins</term>
<term>Plant Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Arabidopsis</term>
<term>Arabidopsis Proteins</term>
<term>Carrier Proteins</term>
<term>Catharanthus</term>
<term>GPI-Linked Proteins</term>
<term>Mitogen-Activated Protein Kinase Kinases</term>
<term>Plant Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Arabidopsis</term>
<term>Catharanthus</term>
<term>Mitogen-Activated Protein Kinase Kinases</term>
<term>Protéines d'Arabidopsis</term>
<term>Protéines de transport</term>
<term>Protéines liées au GPI</term>
<term>Protéines végétales</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Auto-immunité</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Autoimmunity</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Gene Expression Regulation, Plant</term>
<term>Glycosylphosphatidylinositols</term>
<term>MAP Kinase Signaling System</term>
<term>Phosphorylation</term>
<term>Plants, Genetically Modified</term>
<term>RNA Interference</term>
<term>Transcriptome</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Glycosylphosphatidylinositols</term>
<term>Interférence par ARN</term>
<term>Phosphorylation</term>
<term>Régulation de l'expression des gènes végétaux</term>
<term>Système de signalisation des MAP kinases</term>
<term>Transcriptome</term>
<term>Végétaux génétiquement modifiés</term>
</keywords>
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<front><div type="abstract" xml:lang="en">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.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">32978401</PMID>
<DateCompleted><Year>2020</Year>
<Month>10</Month>
<Day>14</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>10</Month>
<Day>16</Day>
</DateRevised>
<Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2041-1723</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>11</Volume>
<Issue>1</Issue>
<PubDate><Year>2020</Year>
<Month>09</Month>
<Day>25</Day>
</PubDate>
</JournalIssue>
<Title>Nature communications</Title>
<ISOAbbreviation>Nat Commun</ISOAbbreviation>
</Journal>
<ArticleTitle>A trimeric CrRLK1L-LLG1 complex genetically modulates SUMM2-mediated autoimmunity.</ArticleTitle>
<Pagination><MedlinePgn>4859</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1038/s41467-020-18600-8</ELocationID>
<Abstract><AbstractText>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.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Huang</LastName>
<ForeName>Yanyan</ForeName>
<Initials>Y</Initials>
<Identifier Source="ORCID">0000-0001-7688-0997</Identifier>
<AffiliationInfo><Affiliation>State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China, Sichuan Agricultural University, 611130, Chengdu, P. R. China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Biochemistry & Biophysics, Institute for Plant Genomics & Biotechnology, Texas A&M University, College Station, TX, 77843, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yin</LastName>
<ForeName>Chuanchun</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China, Sichuan Agricultural University, 611130, Chengdu, P. R. China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Plant Pathology & Microbiology, Institute for Plant Genomics & Biotechnology, Texas A&M University, College Station, TX, 77843, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Jun</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry & Biophysics, Institute for Plant Genomics & Biotechnology, Texas A&M University, College Station, TX, 77843, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Feng</LastName>
<ForeName>Baomin</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry & Biophysics, Institute for Plant Genomics & Biotechnology, Texas A&M University, College Station, TX, 77843, USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>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, 350002, Fuzhou, P. R. China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ge</LastName>
<ForeName>Dongdong</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology & Microbiology, Institute for Plant Genomics & Biotechnology, Texas A&M University, College Station, TX, 77843, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kong</LastName>
<ForeName>Liang</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry & Biophysics, Institute for Plant Genomics & Biotechnology, Texas A&M University, College Station, TX, 77843, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ortiz-Morea</LastName>
<ForeName>Fausto Andres</ForeName>
<Initials>FA</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry & Biophysics, Institute for Plant Genomics & Biotechnology, Texas A&M University, College Station, TX, 77843, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Richter</LastName>
<ForeName>Julia</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Applied Genetics and Cell Biology, University of Natural Resources and Life Sciences, Vienna (BOKU), 18 A-1190, Muthgasse, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hauser</LastName>
<ForeName>Marie-Theres</ForeName>
<Initials>MT</Initials>
<Identifier Source="ORCID">0000-0001-8938-2460</Identifier>
<AffiliationInfo><Affiliation>Department of Applied Genetics and Cell Biology, University of Natural Resources and Life Sciences, Vienna (BOKU), 18 A-1190, Muthgasse, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Wen-Ming</ForeName>
<Initials>WM</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China, Sichuan Agricultural University, 611130, Chengdu, P. R. China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Shan</LastName>
<ForeName>Libo</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology & Microbiology, Institute for Plant Genomics & Biotechnology, Texas A&M University, College Station, TX, 77843, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>He</LastName>
<ForeName>Ping</ForeName>
<Initials>P</Initials>
<Identifier Source="ORCID">0000-0002-5926-8349</Identifier>
<AffiliationInfo><Affiliation>Department of Biochemistry & Biophysics, Institute for Plant Genomics & Biotechnology, Texas A&M University, College Station, TX, 77843, USA. pinghe@tamu.edu.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>R01 GM092893</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 GM097247</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
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<PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
<PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2020</Year>
<Month>09</Month>
<Day>25</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>Nat Commun</MedlineTA>
<NlmUniqueID>101528555</NlmUniqueID>
<ISSNLinking>2041-1723</ISSNLinking>
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<Chemical><RegistryNumber>0</RegistryNumber>
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<Chemical><RegistryNumber>0</RegistryNumber>
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<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<MeshHeading><DescriptorName UI="D058851" MajorTopicYN="N">GPI-Linked Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018506" MajorTopicYN="N">Gene Expression Regulation, Plant</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017261" MajorTopicYN="N">Glycosylphosphatidylinositols</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020930" MajorTopicYN="N">MAP Kinase Kinase Kinases</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020935" MajorTopicYN="N">MAP Kinase Signaling System</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020929" MajorTopicYN="N">Mitogen-Activated Protein Kinase Kinases</DescriptorName>
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<MeshHeading><DescriptorName UI="D010766" MajorTopicYN="N">Phosphorylation</DescriptorName>
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<MeshHeading><DescriptorName UI="D010940" MajorTopicYN="N">Plant Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
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<MeshHeading><DescriptorName UI="D030821" MajorTopicYN="N">Plants, Genetically Modified</DescriptorName>
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<MeshHeading><DescriptorName UI="D034622" MajorTopicYN="N">RNA Interference</DescriptorName>
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A trimeric CrRLK1L-LLG1 complex genetically modulates SUMM2-mediated autoimmunity.

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

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