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一种正向调节因子CsPR10-9赋予茶树对炭疽病(胶孢炭疽菌)的抗性,该调节因子受到茶树中CsMYB72的负调控。

A Positive Regulator CsPR10-9 Confers Resistance to Anthracnose (Colletotrichum gloeosporioides) Is Negatively Regulated by CsMYB72 in Tea Plants.

作者信息

Tao Yongning, Wang Pengke, Gong Yilin, Xu Linlin, Wu Jun, Wang Aoni, Wang Ling, Hu Jianbing, Dong Kun, Zhu Junyan, Wei Chaoling, Liu Shengrui

机构信息

State Key Laboratory of Tea Plant Germplasm Innovation and Resource Utilization, Anhui Agricultural University, Hefei, China.

出版信息

Plant Cell Environ. 2025 Sep;48(9):6965-6981. doi: 10.1111/pce.15676. Epub 2025 Jun 11.

Abstract

Anthracnose is a devastating fungal disease in tea plants caused by the pathogen Colletotrichum species. It severely affects tea yield and quality. Pathogenesis-related (PR) genes play indispensable roles in plant resistance to fungal pathogens. Our transcriptome data showed that PR10 family genes are involved in the immune response to anthracnose infection in tea plants; however, the underlying regulatory mechanisms remain unclear. Here, we identified a PR10 family gene, CsPR10-9, which was highly induced by Colletotrichum gloeosporioides infection and salicylic acid (SA)/methyl jasmonate (MeJA) treatments. Transient silencing of CsPR10-9 substantially compromised the disease resistance of tea plants, and this was accompanied by reduced activities of the antioxidant enzymes, peroxidase (POD) and superoxide dismutase (SOD), resulting in elevated reactive oxygen species (ROS) levels, decreased SA content, and increased jasmonic acid (JA) content. Transient overexpression of CsPR10-9 in tobacco leaves showed that the lesion area on CsPR10-9-overexpressing leaves was significantly smaller than the control leaves, accompanied by decreased HO level and increased POD and SOD activities. CsPR10-9 was negatively regulated by an R2R3-type MYB transcription factor, CsMYB72, which directly bound to MYB transcription factor binding site cis-acting elements in its promoter to inhibit the expression of CsPR10-9. CsMYB72 is localised in the nucleus and participate in the response to anthracnose infection and SA/MeJA treatment. Moreover, silencing of CsMYB72 significantly enhanced disease resistance, increased POD and SOD activities, reduced ROS levels, increased SA content, and decreased JA content. Taken together, our results revealed that the CsMYB72-CsPR10-9 module regulates the SA/JA-mediated defence response of tea plants to anthracnose. This study provides new molecular targets and a theoretical foundation for breeding of disease-resistant tea germplasms.

摘要

炭疽病是由炭疽菌属病原菌引起的茶树毁灭性真菌病害。它严重影响茶叶产量和品质。病程相关(PR)基因在植物对真菌病原体的抗性中发挥着不可或缺的作用。我们的转录组数据表明,PR10家族基因参与茶树对炭疽病感染的免疫反应;然而,其潜在的调控机制仍不清楚。在这里,我们鉴定了一个PR10家族基因CsPR10-9,它在胶孢炭疽菌感染以及水杨酸(SA)/茉莉酸甲酯(MeJA)处理下被高度诱导。CsPR10-9的瞬时沉默显著损害了茶树的抗病性,同时伴随着抗氧化酶过氧化物酶(POD)和超氧化物歧化酶(SOD)活性的降低,导致活性氧(ROS)水平升高、SA含量降低以及茉莉酸(JA)含量增加。CsPR10-9在烟草叶片中的瞬时过表达表明,过表达CsPR10-9的叶片上的病斑面积明显小于对照叶片,同时伴随着HO水平降低以及POD和SOD活性增加。CsPR10-9受到一个R2R3型MYB转录因子CsMYB72的负调控,CsMYB72直接结合到其启动子中的MYB转录因子结合位点顺式作用元件上,以抑制CsPR10-9的表达。CsMYB72定位于细胞核中,并参与对炭疽病感染和SA/MeJA处理的反应。此外,CsMYB72的沉默显著增强了抗病性,增加了POD和SOD活性,降低了ROS水平,增加了SA含量,并降低了JA含量。综上所述,我们的结果表明CsMYB72-CsPR10-9模块调节茶树对炭疽病的SA/JA介导的防御反应。本研究为抗病茶种质资源的培育提供了新的分子靶点和理论基础。

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