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Loss of the Common Immune Coreceptor BAK1 Leads to NLR-dependent Cell Death

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Specialty Science
Date 2020 Oct 15
PMID 33055218
Citations 23
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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 However, double mutants made by and its closest paralog 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 is suppressed when a group of s, s, are mutated, indicating the cell-death of is the consequence of NLR activation. Furthermore, introduction of a 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 s-dependent manner. Our study thus pinpoints that BAK1 and its paralogs are likely guarded by NLRs.

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