植物学报 ›› 2025, Vol. 60 ›› Issue (5): 722-733.DOI: 10.11983/CBB25088 cstr: 32102.14.CBB25088
粟思琳1,2, 唐先宇1,2, 陈祎1,2, 王婷1,2, 夏石头1,2,*()
收稿日期:
2025-05-19
接受日期:
2025-07-08
出版日期:
2025-09-10
发布日期:
2025-07-08
通讯作者:
夏石头
基金资助:
Su Silin1,2, Tang Xianyu1,2, Chen Yi1,2, Wang Ting1,2, Xia Shitou1,2,*()
Received:
2025-05-19
Accepted:
2025-07-08
Online:
2025-09-10
Published:
2025-07-08
Contact:
Xia Shitou
摘要: 系统获得性抗性(SAR)是植物重要的防御机制, 可显著增强植株对病原微生物的抗性, 且具有系统性、持久性和广谱性特征, 其转录调控为抗性激活的核心环节。该文从水杨酸(SA)和Pip/NHP的合成, NPR1、NPR3/NPR4受体和Pip/NHP移动信号等的转录调控, 以及TGA和WRKY转录因子家族调控等方面综述了SAR的转录调控研究进展, 为深入理解植物免疫调控网络以及系统探究植物在复杂环境中平衡生长与防御的机制提供参考。
粟思琳, 唐先宇, 陈祎, 王婷, 夏石头. 植物系统获得性抗性的转录调控. 植物学报, 2025, 60(5): 722-733.
Su Silin, Tang Xianyu, Chen Yi, Wang Ting, Xia Shitou. Transcriptional Regulation of Systemic Acquired Resistance in Plants. Chinese Bulletin of Botany, 2025, 60(5): 722-733.
图1 植物系统获得性抗性(SAR)的转录调控 当病原体(细菌或真菌)侵染植物局部叶片细胞或施用水杨酸(SA)时, 局部信号被感知后, 受体样激酶(RLKs)激活导致钙离子内流, 钙离子与钙调蛋白CAM1/4/6结合后与CBP60g蛋白互作, 通过苯丙氨酸解氨酶(PAL)途径和异分支酸合酶1 (ICS1)途径促进SA的合成, 引发局部抗性反应。而赖氨酸经ALD1和SARD4催化生成哌啶酸(Pip), 再由FMO1羟基化生成N-羟基哌啶酸(NHP), 而Pip/NHP可通过韧皮部转运至远端叶片。随着系统叶细胞中SA和Pip/NHP水平上升, SA与受体NPR1结合, 触发NPR1构象变化并入核, 进而与TGA2/5/6形成复合体, 激活PRs基因表达和SAR反应。同时, SA也能直接结合NPR3/NPR4, 抑制它们的转录抑制活性, 从而解除对SARD1和WRKY70等的抑制, 达到精细调控SAR的目的。实线箭头表示直接调控; 虚线箭头表示间接调控; T型线表示抑制作用。
Figure 1 Transcriptional regulation of systemic acquired resistance (SAR) in plants When local leaf cells of plants are infected by pathogens (bacteria or fungi) or salicylic acid (SA), is applied receptor like kinases (RLKs) are activated after local signal perception, leading to the influx of calcium ions. The calmodulin CAM1/4/6 then combines with calcium ions and interacts with CBP60g, triggeringa local resistance response through the phenylalanine ammonia-lyase (PAL) and isochorismate synthase 1 (ICS1) pathways to increase SA synthesis. Lysine, whereas, is catalyzed by ALD1 and SARD4 to form piperidine-2-carboxylic acid (Pip), which is then hydroxylated to N-hydroxy-piperidine-2-carboxylic acid (NHP) by FMO1. Pip/NHP can be transported to distal leaves through phloem transportation. After the levels of SA and Pip/NHP increase in systemic leaf cells, SA binds to the receptor NPR1, and triggers the conformational changes in NPR1, which enter into the nucleus, where NPR1 forms a complex with TGA2/5/6, and activates the expression of PRs genes and SAR. Moreover, SA can also directly bind NPR3/NPR4 to inhibit their transcriptional inhibitory activity, thereby relieving the inhibition of genes such as SARD1 and WRKY70, achieving the goal of fine tuning the SAR. The solid arrows indicate direct regulation; the dashed arrows indicate indirect regulation; the T-shaped line indicates inhibition.
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