Original data for Co-Immunoprecipitations from "The Arabidopsis TIR-NBS-LRR CSA1 guards BAK1 BIR3 homeostasis and mediates pattern- and effector-induced plant immune responses"

Arabidopsis BAK1/SERK3, a co-receptor of leucine-rich repeat pattern recognition receptors (PRR), mediates pattern-triggered immunity (PTI). Genetic inactivation of BAK1 or BAK1-interacting receptors (BIR) causes cell death. We found that the TIR-NBS-LRR protein CONSTITUTIVE SHADE-AVOIDANCE 1 (CSA1) physically interacts with BIR3, but not with BAK1. Cell death in bak1-4 and bak1-4 bir3-2 mutants is dependent on CSA1 and on components of effector-triggered immunity-(ETI) pathways, including EDS1, PAD4, and the plant hormone, salicylic acid. Effector HopB1-mediated perturbation of BAK1 also results in CSA1-dependent cell death. Likewise, microbial pattern pg23-induced cell death, but not PTI responses, require CSA1. Thus, CSA1 integrates pattern- and effector-mediated cell death pathways downstream of BAK1. CSA1 guards BIR3 BAK1 homeostasis, and de-repression of CSA1 in the absence of intact BAK1 and BIR3 triggers ETI cell death. This suggests that PTI and ETI pathways are activated downstream of BAK1 for efficient plant immunity.

拟南芥（Arabidopsis）BAK1/SERK3作为富亮氨酸重复序列模式识别受体（leucine-rich repeat pattern recognition receptors, PRR）的共受体，介导模式触发免疫（pattern-triggered immunity, PTI）。对BAK1或BAK1互作受体（BAK1-interacting receptors, BIR）进行遗传失活，会引发细胞死亡现象。本研究发现，TIR-NBS-LRR蛋白组成型避荫1（CONSTITUTIVE SHADE-AVOIDANCE 1, CSA1）可与BIR3发生物理互作，但无法结合BAK1。bak1-4与bak1-4 bir3-2突变体中的细胞死亡，依赖于CSA1以及效应子触发免疫（effector-triggered immunity, ETI）通路的相关组分，包括EDS1、PAD4与植物激素水杨酸（salicylic acid）。效应子HopB1介导的BAK1扰动，同样会引发依赖于CSA1的细胞死亡。与之类似，微生物模式分子pg23诱导的细胞死亡（而非PTI响应）也需要CSA1的参与。综上，CSA1可整合BAK1下游的模式介导与效应子介导的细胞死亡通路。CSA1负责维持BIR3与BAK1的稳态，在完整BAK1与BIR3缺失的情况下，CSA1的去抑制会触发ETI型细胞死亡。这一结果表明，PTI与ETI通路可在BAK1下游被激活，从而实现高效的植物免疫。