Li Yilin, Gou Xiuhong, Ma Ruize, Zhang Peiling, Ansabayeva Assiya, Shi Qingyao, Liu Zeming, Meng Yuling, Shan Weixing
State Key Laboratory of Crop Stress Resistance and High-Efficiency Production, and College of Agronomy, Northwest A&F University, Yangling, Shaanxi, 712100, China.
State Key Laboratory of Crop Stress Resistance and High-Efficiency Production, and College of Plant Protection, Northwest A&F University, Yangling, Shaanxi, 712100, China.
Plant J. 2025 Jan;121(2):e17194. doi: 10.1111/tpj.17194. Epub 2024 Dec 5.
Small RNAs are involved in diverse cellular processes, including plant immunity to pathogens. Here, we report that miR158a negatively regulates plant immunity to the oomycete pathogen Phytophthora parasitica in Arabidopsis thaliana. By performing real-time quantitative PCR, transient expression, and RNA ligase-mediated 5' rapid amplification of cDNA ends assays, we demonstrate that miR158a downregulates AtTN7 expression by cleaving its 3'-untranslated region. AtTN7 positively affects plant immunity and encodes a truncated intracellular nucleotide-binding site and leucine-rich repeat receptor containing the Toll/interleukin-1 receptor. AtTN7 can degrade oxidized forms of nicotinamide adenine dinucleotide (NAD+). Further genetic and molecular analyses reveal that the Enhanced Disease Susceptibility 1-Phytoalexin Deficient 4-Activated Disease Resistance 1 complex is required for AtTN7-mediated immunity. ADR1-dependent Ca influx is crucial for activating salicylic acid signaling to condition AtTN7-triggered immunity. Our study uncovers the immune roles and regulatory mechanisms of miR158a and its target AtTN7. Both miR158a-downregulation and AtTN7-overexpression lead to enhanced plant resistance to P. parasitica without affecting plant growth phenotypes, suggesting their application potentials and the utilization of miRNAs in identifying novel immune genes for the development of plant germplasm resources with enhanced disease resistance.
小RNA参与多种细胞过程,包括植物对病原体的免疫。在此,我们报道miR158a在拟南芥中负向调节植物对卵菌病原体寄生疫霉的免疫。通过进行实时定量PCR、瞬时表达和RNA连接酶介导的5' cDNA末端快速扩增分析,我们证明miR158a通过切割AtTN7的3'非翻译区来下调其表达。AtTN7对植物免疫有正向影响,编码一个截短的细胞内核苷酸结合位点和富含亮氨酸重复序列的受体,该受体含有Toll/白细胞介素-1受体。AtTN7可以降解氧化型烟酰胺腺嘌呤二核苷酸(NAD+)。进一步的遗传和分子分析表明,增强的疾病易感性1-植物抗毒素缺陷4-激活的抗病性1复合物是AtTN7介导的免疫所必需的。依赖ADR1的Ca2+内流对于激活水杨酸信号以调节AtTN7触发的免疫至关重要。我们的研究揭示了miR158a及其靶标AtTN7的免疫作用和调控机制。miR158a下调和AtTN7过表达均导致植物对寄生疫霉的抗性增强,而不影响植物生长表型,这表明它们的应用潜力以及利用miRNA鉴定新的免疫基因以开发抗病性增强的植物种质资源。