The Sainsbury Laboratory, University of East Anglia, Norwich Research Park, Norwich, United Kingdom.
PLoS Genet. 2022 Sep 22;18(9):e1010414. doi: 10.1371/journal.pgen.1010414. eCollection 2022 Sep.
Cell surface pattern recognition receptors (PRRs) activate immune responses that can include the hypersensitive cell death. However, the pathways that link PRRs to the cell death response are poorly understood. Here, we show that the cell surface receptor-like protein Cf-4 requires the intracellular nucleotide-binding domain leucine-rich repeat containing receptor (NLR) NRC3 to trigger a confluent cell death response upon detection of the fungal effector Avr4 in leaves of Nicotiana benthamiana. This NRC3 activity requires an intact N-terminal MADA motif, a conserved signature of coiled-coil (CC)-type plant NLRs that is required for resistosome-mediated immune responses. A chimeric protein with the N-terminal α1 helix of Arabidopsis ZAR1 swapped into NRC3 retains the capacity to mediate Cf-4 hypersensitive cell death. Pathogen effectors acting as suppressors of NRC3 can suppress Cf-4-triggered hypersensitive cell-death. Our findings link the NLR resistosome model to the hypersensitive cell death caused by a cell surface PRR.
细胞表面模式识别受体（PRRs）激活免疫反应，其中可能包括超敏细胞死亡。然而，将 PRRs 与细胞死亡反应联系起来的途径尚不清楚。在这里，我们表明，细胞表面受体样蛋白 Cf-4 需要细胞内核苷酸结合域富含亮氨酸重复序列的受体（NLR）NRC3，以在检测到真菌效应物 Avr4 后在 Nicotiana benthamiana 的叶片中引发融合细胞死亡反应。这种 NRC3 活性需要完整的 N 端 MADA 基序，这是卷曲螺旋（CC）型植物 NLR 的保守特征，对于抗病体介导的免疫反应是必需的。具有拟南芥 ZAR1 的 N 端α1 螺旋交换的嵌合蛋白保留介导 Cf-4 超敏细胞死亡的能力。作为 NRC3 抑制剂的病原体效应子可以抑制 Cf-4 触发的超敏细胞死亡。我们的发现将 NLR 抗病体模型与细胞表面 PRR 引起的超敏细胞死亡联系起来。
