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

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.

Transcriptional activation and phosphorylation of OsCNGC9 confer enhanced chilling tolerance in rice

“…It is worth noting that tobacco mosaic virus resistance conferred by the N gene is temperature sensitive (Takabatake et al, 2006). Another recent study showed that the lesion-mimic phenotype of bak1 is dependent on ADR1s, a group of NLRs (Wu et al, 2020). Because the cds1 mutant has no lesion-mimic phenotype at the seedling stage, OsSAPK8, a homolog of Arabidopsis OST1, is inactive under normal temperature conditions, and the channel activity of OsCNGC9 is relatively low to maintain a resting [Ca 2+ ] cyt level.…”

A mis‐regulated cyclic nucleotide‐gated channel mediates cytosolic calcium elevation and activates immunity in Arabidopsis

“…4) is reminiscent of ETI triggered by Arabidopsis CNL RPS2 recognizing Pst delivered effector AvrRpt2, as RPS2‐mediated restriction of bacterial growth was abolished in an eds1 sid2 double mutant (Venugopal et al ., 2009; Cui et al ., 2017; Bhandari et al ., 2019). It was recently shown that cell death in bak1 bkk1 requires a sub‐group of ‘helper’ NLRs (ADR1s) , suggesting that bak1 bkk1 cell death is a consequence of NLR activation (Wu et al ., 2020). These data and our findings raise the question for future work of whether perturbed CNGC Ca 2+ channel activity and/or elevated cytosolic Ca 2+ in cngc20‐4 induces certain NLRs to mobilize ETI responses.…”

The TIR-NBS-LRR protein CSA1 is required for autoimmune cell death in Arabidopsis pattern recognition co-receptorbak1andbir3mutants

“…Since then, multiple components that are necessary for the execution of the bak1 -mediated cell death have been revealed. In suppressor screens, often the double mutant bak1-3 bkk1 and bak1-4 bkk1 were used as the loss of the two closely related SERK family members results in a strong autoimmune cell death phenotype associated with severe dwarfism or even seedlings lethality (He et al, 2007; Albrecht et al, 2008; Schwessinger et al, 2011; de Oliveira et al, 2016; Du et al, 2016; Gao et al, 2017; Wu et al, 2020). The following components have been shown to suppress BAK1 or BIR cell death: ER quality control components such as ENDOPLASMIC RETICULUM DNAJ DOMAIN-CONTAINING PROTEIN 3B (ERdj3b) and STROMAL CELL-DERIVED FACTOR 2 (SDF2) (Sun et al, 2014), the protein glycosylation machinery component STAUROSPORIN AND TEMPERATURE SENSITIVE3 (STT3a) protein (de Oliveira et al, 2016), the cyclic nucleotide gated ion channel 20 (CNGC20) (Yu et al, 2019), the nucleocytoplasmic trafficking component SUPPRESSOR OF BAK1 BKK1/ NUCLEOPORIN 85 (SBB1/NUP85) and the DEAD-box RNA helicase 1 (DRH1) (Du et al, 2016) and the helper NLR family ADR1 (Wu et al, 2020).…”

“…. Recently Wu et al (2020) revealed the helper NLR ADR1 family as part of the bak1 bkk1 cell death pathway. These data indicate that NLR signaling is involved in bak1 - and maybe also bir -mediated cell death.…”