凝集素受體激 LecRK-V.2 和 LecRK-VII.1 參與氣孔免疫及非生物逆境透過組蛋白乙醯轉移1敏化阿拉伯芥模式誘發免疫之研究

Abstract

在自然中，植物氣孔常被做為病原細菌入侵的入口。然而，植物可藉由透過膜受體來感知病原細菌並誘導氣孔之關閉。其中，大多數凝集素受器激(LecRKs) 會受病原菌及病原菌相關分子模式所啟動(PAMPs)。在本研究中，我們發現lecrk-V.2 及lecrk-VII.1 突變株之氣孔關閉對於細菌行斑點病(Pst DC3000) 及病原細菌鞭毛(flg22) 受損。除此之外，增量表現之LecRK-V.2 及LecRK-VII.1 之氣孔關閉對於Flg22 較為敏感、並延緩受Pst DC3000造成的氣孔重新開啟。在lecrk-V.2 及lecrk-VII.1 的突變株之氣孔關閉能力，對於甲基茉莉酸(MeJA) 較為不敏感。在雙分子螢光互補(BiFC) 及免疫共沉澱(CoIP) 中發現LecRK-V.2及LecRK-VII.1 會和細菌鞭毛受體(FLS2) 結合。本研究表明LecRK-V.2 and LecRK-VII.1 參與氣孔免疫並且參與在鞭毛受體及共受體FLS2-BAK1 複合體中。 除此之外，本研究也發現阿拉伯芥如何因非生物逆境影響，而調控對於細菌行斑點病之致病性。受過7 天之鹽、熱、寒害逆境之阿拉伯芥能提高對於細菌病害之感染。並發現逆境下提升抗性之阿拉伯芥之原因是和預先準備免疫有所關聯，並且預先準備先天免疫之啟動是透過RNAPII 調控之轉錄影響。除此，阿拉伯芥在此逆境下會提升免疫相關基因之組蛋白H3K4之二甲基及三甲基化的能力。進一步研究發現，在乙烯基轉移(hac1-1 ) 突變株中並無法誘導，表明預先準備免疫和組蛋白之轉錄後修飾之關聯性。在本次研究中結果表明，植物中的組蛋白修飾和預先準備免疫之間的運作方式。

Stomata act as natural ports for bacterial entry. However, plants can sense biotic invasion through plasma membrane localized receptors and stomatal closure is one of the first innate immunity responses activated upon bacterial infection. Most lectin receptor kinases (LecRKs) are induced in response to pathogens or pathogen-associated molecular patterns (PAMPs). Here, we observed impaired stomatal closure upon infection with bacteria Pst DC3000 or after treatment with the PAMP flg22 in lecrk-V.2 and lecrk-VII.1 mutants. In addition, stomata of transgenic lines over-expressing LecRK-V.2 and LecRK-VII.1 were hypersensitive to flg22 and showed delayed stomatal reopening upon Pst DC3000 inoculation. Stomata of mutants lecrk-V.2 and lecrk-VII.1 were also insensitive to MeJA. Furthermore, BiFC and CoIP data demonstrated association of LecRK-V.2 and LecRK-VII.1 with FLS2. Overall these data suggest that LecRK-V.2 and LecRK-VII.1 are involved in stomatal immunity and are part of the FLS2-BAK1 pattern-recognition receptor complex. In addition, I also evaluated how mild abiotic stresses modulate Arabidopsis resistance to hemi-biotroph Pst DC3000. Arabidopsis exposed to salt, heat or cold stresses for 7 days were more resistant to bacteria infection. Enhanced resistance was correlated with a primed immunity in Arabidopsis exposed to stresses. Priming of innate immunity was associated with RNAPII mediated transcription. Furthermore, Arabidopsis exposed to recurrent stresses showed enrichment of H3K4 dimethylation and trimethylation at immunity-responsive genes. In addition, priming of immunity-responsive genes was not observed in histone acetyltrans-ferase 1-1 (hac1-1 ) mutants after repetitive abiotic stress treatments, further suggesting that primed immunity is related to post translational histone modification. Taken together this work suggests a mechanistic link between histone modifications and the primed state in plants.