Li Qian, Chen Yi, Wei Yingying, Jiang Shu, Ye Jianfen, Chen Jiahui, Xu Feng, Shao Xingfeng
State Key Laboratory for 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, China.
Plant Biotechnol J. 2025 Sep;23(9):3524-3539. doi: 10.1111/pbi.70177. Epub 2025 Jun 4.
Transcription factors MYC2 and JAMs play a crucial role in regulating disease resistance in model plants. However, their regulatory mechanisms of disease resistance in non-model plants, particularly in postharvest fruits, remain largely unknown. In this study, we observed that PpMYC2 expression was up-regulated in peach fruit following infection by Monilinia fructicola, while the expressions of PpJAM2/3 were down-regulated. Furthermore, we found that PpMYC2 positively regulated the resistance against M. fructicola, whereas PpJAM2/3 negatively regulated it. Through a combined DNA affinity purification and RNA sequencing analysis for PpMYC2, we identified lignin synthesis genes (PpPAL1, PpC4H, Pp4CL1, PpCSE and PpCCoAOMT1) as candidate target genes. Subsequent assays, including dual-luciferase reporter assay, transient overexpression and silencing assays, electrophoretic mobility shift assay and yeast one-hybrid assay demonstrated that PpMYC2 activated the transcription of these five genes by binding to their promoters, promoting lignin accumulation. Conversely, PpJAM2 inhibited the transcription of PpC4H and PpCSE, while PpJAM3 inhibited Pp4CL1 and PpCCoAOMT1. Additionally, PpJAM2 or PpJAM3 interfered with PpMYC2's activation of their common target genes by competitively binding to the promoters. In conclusion, when peach fruit is infected with M. fructicola, up-regulation of PpMYC2 promotes lignin synthesis, while down-regulation of PpJAM2/3 reduces their inhibitory effects, ultimately resulting in lignin accumulation to combat the disease infection. Our study provides new insights into the molecular mechanisms of disease response in postharvest peach fruit.
转录因子MYC2和JAMs在调控模式植物的抗病性中发挥着关键作用。然而，它们在非模式植物，尤其是采后果实中的抗病调控机制仍 largely未知。在本研究中，我们观察到桃果实被褐腐病菌感染后，PpMYC2的表达上调，而PpJAM2/3的表达下调。此外，我们发现PpMYC2正向调控对褐腐病菌的抗性，而PpJAM2/3负向调控该抗性。通过对PpMYC2进行DNA亲和纯化和RNA测序分析相结合，我们鉴定出木质素合成基因（PpPAL1、PpC4H、Pp4CL1、PpCSE和PpCCoAOMT1）作为候选靶基因。随后的实验，包括双荧光素酶报告基因检测、瞬时过表达和沉默检测、电泳迁移率变动分析和酵母单杂交检测，表明PpMYC2通过结合这些基因的启动子激活其转录，促进木质素积累。相反，PpJAM2抑制PpC4H和PpCSE的转录，而PpJAM3抑制Pp4CL1和PpCCoAOMT1的转录。此外，PpJAM2或PpJAM3通过竞争性结合启动子干扰PpMYC2对其共同靶基因的激活。总之，桃果实被褐腐病菌感染时，PpMYC2的上调促进木质素合成，而PpJAM2/3的下调降低其抑制作用，最终导致木质素积累以抵抗病害感染。我们的研究为采后桃果实病害反应的分子机制提供了新的见解。
