2017年3月16日， 國際著名學術雜誌《Cell》子刊《Current Biology》雜誌線上發表了南京農業大學植物保護學院作物疫病研究團隊王源超教授、董莎萌教授和美國加州大學河濱分校Wenbo Ma教授合作的題為《A Phytophthora effector manipulates host histone acetylation and reprograms defense gene expression to promote infection》的一項最新研究成果， 博士生孔亮為論文第一作者， 長江學者王源超教授和青年千人董莎萌教授為論文通訊作者。
組蛋白修飾(Histone modification)是生物體表觀遺傳修飾的一種重要方式， 通過影響基因表達、染色質重塑等過程廣泛參與生物體的生長、發育及免疫等方面。 本研究發現大豆疫黴分泌的效應蛋白Avh23能夠進入到大豆細胞內， 通過競爭性結合組蛋白乙醯化修飾複合體SAGA的ADA2亞基，
王源超教授研究團隊以發展作物疫病防控新策略與新技術為目標， 長期聚焦於作物疫病的致病機制， 從不同角度與層次研究疫黴菌“攻擊”和植物“抵抗”的過程與規律， 在作物對疫黴菌的基礎抗性、疫黴菌利用效應子攻擊植物的分子機理、植物對疫黴菌的特異抗性及效應子變異導致的植物抗性喪失機制等方面取得了一系列重要進展。
原文連結：
原文摘要:
Immune response during pathogen infection requires extensive transcription reprogramming. A fundamental mechanism of transcriptional regulation is histone acetylation. However, how pathogens interfere with this process to promote disease remains largely unknown. Here we demonstrate that the cytoplasmic effector PsAvh23 produced by the soybean pathogen Phytophthora sojae acts as a modulator of histone acetyltransferase (HAT) in plants. PsAvh23 binds to the ADA2 subunit of the HAT complex SAGA and disrupts its assembly by interfering with the association of ADA2 with the catalytic subunit GCN5. As such, PsAvh23 suppresses H3K9 acetylation mediated by the ADA2/GCN5 module and increases plant susceptibility. expression of PsAvh23 or silencing of GmADA2/GmGCN5resulted in misregulation of defense-related genes, most likely due to decreased H3K9 acetylation levels at the corresponding loci. This study highlights an effective counter-defense mechanism by which a pathogen effector suppresses the activation of defense genes by interfering with the function of the HAT complex during infection.