桃褐腐病菌Mona元件调控MfCYP51基因超量表达的分子机理研究

褐腐病是桃生产中最为严重的病害之一。前期研究发现褐腐病菌Monilinia fructicola抗性菌株MfCYP51基因的上游存在一个具有启动子活性的Mona元件，可以上调MfCYP51基因表达从而使病菌获得对DMI杀菌剂的抗性。本研究拟利用Reverse-ChIP方法，对与Mona互作的转录因子进行筛选及鉴定。通过遗传转化对筛选到的转录因子编码基因进行敲除以解析其生物学功能。同时通过酵母双杂交筛选Mona转录因子的互作蛋白，明确Mona及其转录因子的调控网络，阐明Mona调控下游基因超量表达的分子机理。本项目的顺利实施不仅可以阐明Mona元件调控褐腐病菌对DMI杀菌剂抗性的分子机理，同时抗性调控相关转录因子有望作为药物设计分子靶标，对高效治理抗DMI杀菌剂的褐腐病菌群体具有重要的实践价值。

Brown rot disease caused by Monilinia fructicola is one of the most important disease in peach production. Previous studies showed that there was a Mona element at the upstream of the MfCYP51 gene in DMI resistant M. fructicola isolates. This element has the promoter activity and causes the DMI fungicide resistance via over-expression of the downstream MfCYP51 gene. In this project, the transcription factors (TFs) interacting with Mona element will be screened and identified by using Reverse-ChIP analysis. The biological functions of the identified TF-encoding genes will be investigated through genetic knockout manipulation. At the same time, the proteins interacting with Mona TFs will be screened through yeast-two-hybrid system to demonstrate the molecualr mechanisms of Mona element for up-regulating the downstream genes. This project is not only scientifically significant, the resulted TFs may be used as molecular targets for designing fungicides in management of the DMI resistant M. fructicola population.