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Activation of the BABA-induced priming defence through redox homeostasis and the modules of TGA1 and MAPKK5 in postharvest peach fruit
Molecular Plant Pathology ( IF 4.8 ) Pub Date : 2021-09-08 , DOI: 10.1111/mpp.13134
Chunhong Li 1, 2 , Kaituo Wang 1, 2 , Yixiao Huang 3 , Changyi Lei 1 , Shifeng Cao 4 , Linglan Qiu 1 , Feng Xu 2, 5 , Yongbo Jiang 1 , Yanyu Zou 1 , Yonghua Zheng 2
Affiliation  

The priming of defence responses in pathogen-challenged model plants undergoes a preparation phase and an expression phase for defence function. However, the priming response in postharvest fruits has not been elucidated. Here, we found that 50 mM β-aminobutyric acid (BABA) treatment could induce two distinct pathways linked with TGA1-related systemic acquired resistance (SAR), resulting in the alleviation of Rhizopus rot in postharvest peach fruit. The first priming phase was elicited by BABA alone, leading to the enhanced transcription of redox-regulated genes and posttranslational modification of PpTGA1. The second phase was activated by an H2O2 burst via up-regulation of PpRBOH genes and stimulation of the MAPK cascade on pathogen invasion, resulting in a robust defence. In the MAPK cascade, PpMAPKK5 was identified as a shortcut interacting protein of PpTGA1 and increased the DNA binding activity of PpTGA1 for the activation of salicylic acid (SA)-responsive PR genes. The overexpression of PpMAPKK5 in Arabidopsis caused the constitutive transcription of SA-dependent PR genes and as a result conferred resistance against the fungus Rhizopus stolonifer. Hence, we suggest that the BABA-induced priming defence in peaches is activated by redox homeostasis with an elicitor-induced reductive signalling and a pathogen-stimulated H2O2 burst, which is accompanied by the possible phosphorylation of PpTGA1 by PpMAPKK5 for signal amplification.

中文翻译:

采后桃果实通过氧化还原稳态和 TGA1 和 MAPKK5 模块激活 BABA 诱导的启动防御

病原体攻击模式植物中防御反应的启动经历了防御功能的准备阶段和表达阶段。然而,尚未阐明采后水果的引发反应。在这里,我们发现 50 mM β-氨基丁酸 (BABA) 处理可以诱导与 TGA1 相关的系统获得性抗性 (SAR) 相关的两种不同途径,从而减轻采后桃果实中的根霉腐病。第一个启动阶段仅由 BABA 引发,导致氧化还原调节基因的转录增强和 PpTGA1 的翻译后修饰。第二相由 H 2 O 2爆发通过上调PpRBOH 激活基因和 MAPK 级联对病原体入侵的刺激,导致强大的防御。在 MAPK 级联中,PpMAPKK5 被鉴定为 PpTGA1 的快捷相互作用蛋白,并增加了 PpTGA1 的 DNA 结合活性,以激活水杨酸 (SA) 反应性PR基因。PpMAPKK5拟南芥中的过表达导致 SA 依赖性PR基因的组成型转录,结果赋予了对真菌Rhizopus stolonifer的抗性。因此,我们认为 BABA 诱导的桃子启动防御是由氧化还原稳态激活的,具有诱导剂诱导的还原信号和病原体刺激的 H 2 O 2爆发,伴随着 PpMAPKK5 可能磷酸化 PpTGA1 以进行信号放大。
更新日期:2021-11-10
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