表觀遺傳學對於植物病原微生物交互作用之調控探討

Abstract

植物在辨識到微生物所共有且演化保守的分子結構時，將啟動先天性免疫反應，而該種分子結構稱為病原菌相關分子模式(pathogen-associated molecular patterns, PAMPs)。此防禦反應稱之為模式誘發免疫反應(pattern-triggered immunity, PTI)。而這種免疫反應近年來已被發現是經由表觀遺傳的甲基化以及乙醯化調控。為了解植物對抗Pseudomonas syringae (Pst)甲基化調控的機制，我們利用KRYPTONITE (KYP) 這個基因的突變株來做為材料，其是專一性的甲基化組蛋白三第九個賴氨酸的雙甲基化轉位酵素。接種了Pst後，突變株的抗性較為野生種(Col-0)強。突變株中的氣孔免疫能力、防禦基因FRK1以及WRKY22的表現量也較野生種來得高。當處理了病原菌相關分子模式，突變株中組蛋白三第九個賴氨酸的雙甲基化程度在防禦基因FRK1以及WRKY22的雙甲基化程度也大幅的減低。從我們的研究得知，在植物以及病原菌的交互關係中，組蛋白甲基化為相當重要的調控角色。

Pathogen-associated molecular patterns (PAMPs) such as flagellin (flg22) are microbial molecular signatures recognized by pattern recognition receptors (PRRs). Recognition leads to the activation of PAMP-triggered immunity (PTI). Many defense-responsive mechanisms involved in PTI are believe to be under epigenetic control mediated by histone acetylation, histone methylation and DNA methyation modifications. To increase our understanding of Arabidopsis thaliana defense mechanisms towards Pseudomonas syringae bacteria, we studied KRYPTONITE (KYP), a methyltransferase specific to Histone 3 Lysine 9 dimethylation (H3K9me2). Loss of function mutants of KYP demonstrated boosted resistance against Pseudomonas syringae when compared to wild-type controls (Col-0). Notably, priming of PTI marker genes such as FRK1 and WRKY22 were observed after flg22 treatment in kyp mutants. In addition, we found decreased enrichment of H3K9me2 at promoter and ATG region of FRK1 and WRKY22 in Col-0 plants treated with the PAMP flg22. Our results suggest that histone H3 lysine 9 dimethylation is a critical component in the signaling and defense processes occurring between plants and microbes.