Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, USA; Howard Hughes Medical Institute, University of North Carolina at Chapel Hill, Chapel Hill, USA.
ZMBP-Plant Physiology, University of Tübingen, Tübingen, Germany.
Curr Opin Plant Biol. 2019 Aug;50:82-94. doi: 10.1016/j.pbi.2019.03.013. Epub 2019 May 4.
Plant nucleotide-binding domain and leucine-rich repeat-containing (NLR) proteins function as intracellular receptors in response to pathogens and activate effector-triggered immune responses (ETI). The activation of some sensor NLRs (sNLR) by their corresponding pathogen effector is well studied. However, the mechanisms by which the recently defined helper NLRs (hNLR) function to transduce sNLR activation into ETI-associated cell death and disease resistance remains poorly understood. We briefly summarize recent examples of sNLR activation and we then focus on hNLR requirements in sNLR-initiated immune responses. We further discuss how shared sequence homology with fungal self-incompatibility proteins and the mammalian mixed lineage kinase domain like pseudokinase (MLKL) proteins informs a plausible model for the structure and function of an ancient clade of plant hNLRs, called RNLs.
植物核苷酸结合域和富含亮氨酸重复序列的（NLR）蛋白作为细胞内受体，对病原体作出反应并激活效应子触发的免疫反应（ETI）。某些传感器 NLR（sNLR）被其相应的病原体效应物激活的机制已得到充分研究。然而，最近定义的辅助 NLR（hNLR）如何将 sNLR 的激活转导为 ETI 相关细胞死亡和抗病性的机制仍知之甚少。我们简要总结了 sNLR 激活的最新实例，然后重点介绍了 hNLR 在 sNLR 引发的免疫反应中的要求。我们进一步讨论了与真菌自交不亲和蛋白和哺乳动物混合谱系激酶结构域样假激酶（MLKL）蛋白的同源序列共享如何为植物 hNLR 中一个古老的 NLR 家族（称为 RNLs）的结构和功能提供一个合理的模型。
