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Loss of the common immune coreceptor BAK1 leads to NLR-dependent cell death.

Identifieur interne : 000115 ( Main/Exploration ); précédent : 000114; suivant : 000116

Loss of the common immune coreceptor BAK1 leads to NLR-dependent cell death.

Auteurs : Yujun Wu [République populaire de Chine] ; Yang Gao [République populaire de Chine] ; Yanyan Zhan [République populaire de Chine] ; Hong Kui [République populaire de Chine] ; Hongyan Liu [République populaire de Chine] ; Li Yan [République populaire de Chine] ; Birgit Kemmerling [Allemagne] ; Jian-Min Zhou [République populaire de Chine] ; Kai He [République populaire de Chine] ; Jia Li [République populaire de Chine]

Source :

RBID : pubmed:33055218

Abstract

Plants utilize a two-tiered immune system consisting of pattern recognition receptor (PRR)-triggered immunity (PTI) and effector-triggered immunity (ETI) to defend themselves against pathogenic microbes. The receptor protein kinase BAK1 plays a central role in multiple PTI signaling pathways in Arabidopsis However, double mutants made by BAK1 and its closest paralog BKK1 exhibit autoimmune phenotypes, including cell death resembling a typical nucleotide-binding leucine-rich repeat protein (NLR)-mediated ETI response. The molecular mechanisms of the cell death caused by the depletion of BAK1 and BKK1 are poorly understood. Here, we show that the cell-death phenotype of bak1 bkk1 is suppressed when a group of NLRs, ADR1s, are mutated, indicating the cell-death of bak1 bkk1 is the consequence of NLR activation. Furthermore, introduction of a Pseudomonas syringae effector HopB1, which proteolytically cleaves activated BAK1 and its paralogs via either gene transformation or bacterium-delivery, results in a cell-death phenotype in an ADR1s-dependent manner. Our study thus pinpoints that BAK1 and its paralogs are likely guarded by NLRs.

DOI: 10.1073/pnas.1915339117
PubMed: 33055218
PubMed Central: PMC7604517


Affiliations:


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<div type="abstract" xml:lang="en">Plants utilize a two-tiered immune system consisting of pattern recognition receptor (PRR)-triggered immunity (PTI) and effector-triggered immunity (ETI) to defend themselves against pathogenic microbes. The receptor protein kinase BAK1 plays a central role in multiple PTI signaling pathways in
<i>Arabidopsis</i>
However, double mutants made by
<i>BAK1</i>
and its closest paralog
<i>BKK1</i>
exhibit autoimmune phenotypes, including cell death resembling a typical nucleotide-binding leucine-rich repeat protein (NLR)-mediated ETI response. The molecular mechanisms of the cell death caused by the depletion of BAK1 and BKK1 are poorly understood. Here, we show that the cell-death phenotype of
<i>bak1 bkk1</i>
is suppressed when a group of
<i>NLR</i>
s,
<i>ADR1</i>
s, are mutated, indicating the cell-death of
<i>bak1 bkk1</i>
is the consequence of NLR activation. Furthermore, introduction of a
<i>Pseudomonas syringae</i>
effector HopB1, which proteolytically cleaves activated BAK1 and its paralogs via either gene transformation or bacterium-delivery, results in a cell-death phenotype in an
<i>ADR1</i>
s-dependent manner. Our study thus pinpoints that BAK1 and its paralogs are likely guarded by NLRs.</div>
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<i>Arabidopsis</i>
However, double mutants made by
<i>BAK1</i>
and its closest paralog
<i>BKK1</i>
exhibit autoimmune phenotypes, including cell death resembling a typical nucleotide-binding leucine-rich repeat protein (NLR)-mediated ETI response. The molecular mechanisms of the cell death caused by the depletion of BAK1 and BKK1 are poorly understood. Here, we show that the cell-death phenotype of
<i>bak1 bkk1</i>
is suppressed when a group of
<i>NLR</i>
s,
<i>ADR1</i>
s, are mutated, indicating the cell-death of
<i>bak1 bkk1</i>
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<i>Pseudomonas syringae</i>
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<i>ADR1</i>
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