Boyce Thompson Institute for Plant Research, Ithaca, New York, 14853, USA.
Plant Pathology and Plant-Microbe Biology Section, School of Integrative Plant Science, Cornell University, Ithaca, New York, 14853, USA.
Plant J. 2024 Jan;117(1):7-22. doi: 10.1111/tpj.16502. Epub 2023 Oct 16.
Plant intracellular immune receptors, primarily nucleotide-binding, leucine-rich repeat proteins (NLRs), detect pathogen effector proteins and activate NLR-triggered immunity (NTI). Recently, 'sensor' NLRs have been reported to function with 'helper' NLRs to activate immunity. We investigated the role of two helper NLRs, Nrc2 and Nrc3, on immunity in tomato to the bacterial pathogen Pseudomonas syringae pv. tomato (Pst) mediated by the sensor NLR Prf and the Pto kinase. An nrc2/nrc3 mutant no longer activated Prf/Pto-mediated NTI to Pst containing the effectors AvrPto and AvrPtoB. An nrc3 mutant showed intermediate susceptibility between wild-type plants and a Prf mutant, while an nrc2 mutant developed only mild disease. These observations indicate that Nrc2 and Nrc3 act additively in Prf-/Pto-mediated immunity. We examined at what point Nrc2 and Nrc3 act in the Prf/Pto-mediated immune response. In the nrc2/3 mutant, programmed cell death (PCD) normally induced by constitutively active variants of AvrPtoB, Pto, or Prf was abolished, but that induced by M3Kα or Mkk2 was not. PCD induced by a constitutively active Nrc3 was also abolished in a Nicotiana benthamiana line with reduced expression of Prf. MAPK activation triggered by expression of AvrPto in the wild-type tomato plants was completely abolished in the nrc2/3 mutant. These results indicate that Nrc2 and Nrc3 act with Prf/Pto and upstream of MAPK signaling. Nrc2 and Nrc3 were not required for PCD triggered by Ptr1, another sensor NLR-mediating Pst resistance, although these helper NLRs do appear to be involved in resistance to certain Pst race 1 strains.
植物细胞内免疫受体，主要是核苷酸结合，富含亮氨酸重复蛋白（NLRs），检测病原体效应蛋白并激活 NLR 触发免疫（NTI）。最近，据报道“传感器”NLR 与“辅助”NLR 一起发挥作用以激活免疫。我们研究了两个辅助 NLR，Nrc2 和 Nrc3，在番茄对细菌病原体丁香假单胞菌 pv 的免疫中的作用。番茄（Pst）由传感器 NLR Prf 和 Pto 激酶介导。nrc2/nrc3 突变体不再激活含有效应物 AvrPto 和 AvrPtoB 的 Prf/Pto 介导的 NTI。nrc3 突变体在野生型植物和 Prf 突变体之间表现出中间易感性，而 nrc2 突变体仅表现出轻度疾病。这些观察结果表明，Nrc2 和 Nrc3 在 Prf/Pto 介导的免疫中起累加作用。我们检查了 Nrc2 和 Nrc3 在 Prf/Pto 介导的免疫反应中起作用的时间。在 nrc2/3 突变体中，由组成型激活的 AvrPtoB、Pto 或 Prf 的变体诱导的程序性细胞死亡（PCD）被消除，但由 M3Kα 或 Mkk2 诱导的 PCD 未被消除。在 Prf 表达降低的烟草原生质体 line 中，组成型激活的 Nrc3 诱导的 PCD 也被消除。在 nrc2/3 突变体中，表达 AvrPto 在野生型番茄植物中触发的 MAPK 激活完全被消除。这些结果表明，Nrc2 和 Nrc3 与 Prf/Pto 一起作用，并在 MAPK 信号转导的上游起作用。Nrc2 和 Nrc3 不参与由另一个传感器 NLR 介导的 Pst 抗性 Ptr1 触发的 PCD，尽管这些辅助 NLR 似乎确实参与了对某些 Pst 1 菌株的抗性。
