The Arabidopsis RRS1-R Resistance gene confers recognition of the bacterial acetyltransferase PopP2 and another bacterial effector, AvrRps4. The RRS1-S allele recognizes AvrRps4 but not PopP2. RRS1- R/RRS1-S heterozygotes cannot recognize PopP2. RRS1-R and RRS1-S also suppress the constitutive RPS4-dependent autoactivity of RRS1-R^slh1. Phytoplasmas cause important plant diseases, and their effectors can cause degradation of specific host proteins. We tested whether attaching a pathogen effector-dependent degron to RRS1-R, enabling its degradation by phytoplasma effector SAP05, could derepress RRS1-R^slh1 autoactivity, resulting in SAP05-dependent resistance. In transient assays in tobacco, RRS1-R-derived constructs can confer a hypersensitive response (HR) to SAP05. However, phytoplasma infection assays in transgenic Arabidopsis resulted in delayed disease symptoms but not full resistance. We provide a proof-of-concept strategy utilizing the recessiveness of a plant immune receptor gene to engineer recognition of a pathogen effector that promotes degradation of a specific host protein.

中文翻译：

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设计成配对 NLR 复合体的新型效应器识别能力

拟南芥RRS1-R 抗性基因可识别细菌乙酰转移酶 PopP2 和另一种细菌效应子 AvrRps4。该RRS1-S等位基因识别AvrRps4但不PopP2。RRS1-R/RRS1-S杂合子不能识别 PopP2。RRS1-R和RRS1-S还抑制RRS1-R ^slh1的组成型 RPS4 依赖性自身^活性。植原体引起重要的植物病害，其效应物可引起特定宿主蛋白质的降解。我们测试了将病原体效应子依赖的 degron 附加到 RRS1-R 上，使其能够被植原体效应子 SAP05 降解，是否可以抑制 RRS1-R ^slh1自身活性，导致依赖 SAP05 的抗性。在烟草的瞬时检测中，RRS1-R 衍生的构建体可以赋予对 SAP05 的超敏反应 (HR)。然而，转基因拟南芥中的植原体感染检测导致疾病症状延迟，但没有完全抵抗。我们提供了一种概念验证策略，利用植物免疫受体基因的隐性来设计病原体效应子的识别，促进特定宿主蛋白质的降解。