Serveur d'exploration sur les récepteurs immunitaires végétaux

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Atypical Resistance Protein RPW8/HR Triggers Oligomerization of the NLR Immune Receptor RPP7 and Autoimmunity.

Identifieur interne : 000208 ( Main/Exploration ); précédent : 000207; suivant : 000209

Atypical Resistance Protein RPW8/HR Triggers Oligomerization of the NLR Immune Receptor RPP7 and Autoimmunity.

Auteurs : Lei Li [Allemagne] ; Anette Habring [Allemagne] ; Kai Wang [Allemagne] ; Detlef Weigel [Allemagne]

Source :

RBID : pubmed:32101702

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English descriptors

Abstract

In certain plant hybrids, immunity signaling is initiated when immune components interact in the absence of a pathogen trigger. In Arabidopsis thaliana, such autoimmunity and cell death are linked to variants of the NLR RPP7 and the RPW8 proteins involved in broad-spectrum resistance. We uncover the molecular basis for this autoimmunity and demonstrate that a homolog of RPW8, HR4Fei-0, can trigger the assembly of a higher-order RPP7 complex, with autoimmunity signaling as a consequence. HR4Fei-0-mediated RPP7 oligomerization occurs via the RPP7 C-terminal leucine-rich repeat (LRR) domain and ATP-binding P-loop. RPP7 forms a higher-order complex only in the presence of HR4Fei-0 and not with the standard HR4 variant, which is distinguished from HR4Fei-0 by length variation in C-terminal repeats. Additionally, HR4Fei-0 can independently form self-oligomers, which directly kill cells in an RPP7-independent manner. Our work provides evidence for a plant resistosome complex and the mechanisms by which RPW8/HR proteins trigger cell death.

DOI: 10.1016/j.chom.2020.01.012
PubMed: 32101702


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Le document en format XML

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<term>Gene Expression Regulation, Plant (MeSH)</term>
<term>Plant Immunity (MeSH)</term>
<term>Plants, Genetically Modified (MeSH)</term>
<term>Protein Multimerization (MeSH)</term>
<term>Tobacco (immunology)</term>
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<term>Immunité des plantes (MeSH)</term>
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<term>Protéines d'Arabidopsis (immunologie)</term>
<term>Régulation de l'expression des gènes végétaux (MeSH)</term>
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<div type="abstract" xml:lang="en">In certain plant hybrids, immunity signaling is initiated when immune components interact in the absence of a pathogen trigger. In Arabidopsis thaliana, such autoimmunity and cell death are linked to variants of the NLR RPP7 and the RPW8 proteins involved in broad-spectrum resistance. We uncover the molecular basis for this autoimmunity and demonstrate that a homolog of RPW8, HR4
<sup>Fei-0</sup>
, can trigger the assembly of a higher-order RPP7 complex, with autoimmunity signaling as a consequence. HR4
<sup>Fei-0</sup>
-mediated RPP7 oligomerization occurs via the RPP7 C-terminal leucine-rich repeat (LRR) domain and ATP-binding P-loop. RPP7 forms a higher-order complex only in the presence of HR4
<sup>Fei-0</sup>
and not with the standard HR4 variant, which is distinguished from HR4
<sup>Fei-0</sup>
by length variation in C-terminal repeats. Additionally, HR4
<sup>Fei-0</sup>
can independently form self-oligomers, which directly kill cells in an RPP7-independent manner. Our work provides evidence for a plant resistosome complex and the mechanisms by which RPW8/HR proteins trigger cell death.</div>
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<sup>Fei-0</sup>
, can trigger the assembly of a higher-order RPP7 complex, with autoimmunity signaling as a consequence. HR4
<sup>Fei-0</sup>
-mediated RPP7 oligomerization occurs via the RPP7 C-terminal leucine-rich repeat (LRR) domain and ATP-binding P-loop. RPP7 forms a higher-order complex only in the presence of HR4
<sup>Fei-0</sup>
and not with the standard HR4 variant, which is distinguished from HR4
<sup>Fei-0</sup>
by length variation in C-terminal repeats. Additionally, HR4
<sup>Fei-0</sup>
can independently form self-oligomers, which directly kill cells in an RPP7-independent manner. Our work provides evidence for a plant resistosome complex and the mechanisms by which RPW8/HR proteins trigger cell death.</AbstractText>
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<CoiStatement>Declaration of Interests The authors declare no competing interests.</CoiStatement>
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