State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-Products, Zhejiang Key Laboratory of Intelligent Food Logistic and Processing, Zhejiang-Malaysia Joint Research Laboratory for Agricultural Product Processing and Nutrition, College of Food Science and Engineering, Ningbo University, Ningbo 315800, China.
State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-Products, Zhejiang Key Laboratory of Intelligent Food Logistic and Processing, Zhejiang-Malaysia Joint Research Laboratory for Agricultural Product Processing and Nutrition, College of Food Science and Engineering, Ningbo University, Ningbo 315800, China.
Int J Biol Macromol. 2024 Nov;279(Pt 3):135350. doi: 10.1016/j.ijbiomac.2024.135350. Epub 2024 Sep 4.
In plant-pathogen interactions, numerous pathogens secrete polygalacturonase (PG) to degrade plants cell walls, whereas plants produce PG-inhibiting protein (PGIP) that specifically binds to pathogen-derived PG to inhibit its activity and resist pathogen infection. In the present study, we dshowed that PpPGIP1 was significantly upregulated in peaches after Monilinia fructicola infection, and the prokaryotic expression of the PpPGIP1 protein inhibited M. fructicola by mitigating its PG activity. Transient overexpression of PpPGIP1 in peaches significantly enhanced their resistance to M. fructicola. PpPGIP1 promoter had several W-box the defense elements that can bind to WRKY transcription factors. Transcriptome analysis identified 20 differentially expressed WRKY genes, including the classic disease resistance gene WRKY33. PpWRKY33 is significantly upregulated in M. fructicola infected peaches. PpWRKY33 is localized in the nucleus and can bind to the W-box in the PpPGIP1 promoter to transcriptional activate the expression of PpPGIP1. Transient overexpression PpWRKY33 upregulated PpPGIP1 expression in peaches, and silencing PpWRKY33 decreased the PpPGIP1 expression. These results indicated that PpPGIP1 positively regulates fungal disease resistance in peaches and is transcriptionally activated by PpWRKY33. These findings reveal the disease resistant role of PpPGIP1 in peaches, and provide new insights into its transcriptional regulation.
在植物-病原体相互作用中,许多病原体分泌多聚半乳糖醛酸酶(PG)来降解植物细胞壁,而植物则产生 PG 抑制蛋白(PGIP),它特异性地结合病原体衍生的 PG,以抑制其活性并抵抗病原体感染。在本研究中,我们表明,在桃果实感染桃褐腐病菌后,PpPGIP1 显著上调,并且 PpPGIP1 蛋白的原核表达通过减轻其 PG 活性来抑制 M. fructicola。在桃中瞬时过表达 PpPGIP1 显著增强了其对 M. fructicola 的抗性。PpPGIP1 启动子具有几个 W-box 防御元件,可与 WRKY 转录因子结合。转录组分析鉴定了 20 个差异表达的 WRKY 基因,包括经典抗病基因 WRKY33。在受 M. fructicola 感染的桃中,PpWRKY33 显著上调。PpWRKY33 定位于细胞核内,可与 PpPGIP1 启动子中的 W-box 结合,转录激活 PpPGIP1 的表达。瞬时过表达 PpWRKY33 上调了桃中 PpPGIP1 的表达,而沉默 PpWRKY33 则降低了 PpPGIP1 的表达。这些结果表明 PpPGIP1 正向调控桃果实的真菌抗病性,并被 PpWRKY33 转录激活。这些发现揭示了 PpPGIP1 在桃中的抗病作用,并为其转录调控提供了新的见解。