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標題: | 探討阿拉伯芥中一凝集素在β-aminobutyric acid誘導所造成priming現象的功能性分析 Functional analysis of a lectin receptor kinase in BABA-mediated priming |
作者: | Grace Jui-Chih Lin 林瑞治 |
指導教授: | 金洛仁(Laurent Zimmerli) |
關鍵字: | 促發效應,阿拉伯芥,β-aminobutyric acid,凝集素,激酶,受體,逆境,抗病反應, priming,Arabidopsis thaliana,β-aminobutyric acid,lectin,receptor protein kinase,stress,pathogen response, |
出版年 : | 2008 |
學位: | 碩士 |
摘要: | “促發效應”(priming) 是指植物在面對生物和非生物逆境時能啟動更快和更強的防禦反應的一種生理情况。 許多天然物質和人造化合物都可以促使植物進入這樣的一個所謂“警戒狀態”或“促發狀態”,可是這個現象的分子機制到目前為止都還不清楚。 為了辨識參與在這個分子機制的基因,我們使用一種人造化學藥品名叫β-aminobutyric acid,簡稱 BABA,做為研究促發效應的媒介。這種原本不存在植物體本身的物質,不僅幫助植物抵抗各式各樣的生物及非生物逆境,還能在不嚴重影響植物的適應(fitness)下,強化被啟動的防禦反應。根據基因晶片的結果,我們挑選了28個對BABA有特殊反應的基因,並利用有 T-DNA插入的阿拉伯芥的突變株進行BABA所造成根抑制和對抗蕃茄細菌性斑點病病原菌(Pseudomonas syringae pv tomato DC3000) 的反應測試。經過篩選後,一個凝集素激酶受體的突變株 (lecRK-a1)不但對BABA具有更明顯的根抑制情況,對蕃茄細菌性斑點病病原菌也不再保有抗病的效果。失去抗病的現象被認為跟缺乏防禦蛋白質PR-1 (PATHOGENESIS-RELATED 1) 的表現量有很大的關連。 然而,這樣的防禦缺失並沒有在感染其他病原菌中被觀察到。總結來說,這個凝集素激酶受體基因在BABA所誘導對抗蕃茄細菌性斑點病病原菌的抗性是不可獲缺的。 另外,我們觀察到,此基因在原生種被感病的情況下,很快被誘導表現。因此,這個基因極可能是在參與在很上游的植物和微生物戶相辨認的互動中。 “Priming” is defined as a physiological condition in which plants are able to better or more rapidly mount defense responses to biotic or abiotic stresses. Many natural or synthetic compounds can alert plants to enter a so-called ‘alarmed’ or ‘primed state.’ However, the molecular mechanism of priming remains unclear at this moment. To elucidate its mechanism, the priming inducer, β-aminobutyric acid (BABA), was employed as a tool to discover genes involved in priming. The xenobiotic BABA enhances plant resistance to a wide range of biotic and abiotic stresses without a significant tradeoff in plant fitness. Twenty eight Arabidopsis T-DNA insertion lines selected from a group of BABA-responsive genes were tested for their responses to BABA- inhibition of root growth and BABA-induced resistance (BABA-IR) to the virulent bacteria, Pseudomonas syringae pv tomato DC3000 (Pst DC3000). A lectin receptor kinase mutant (lecRK-a1) demonstrated enhanced BABA-mediated root growth inhibition and a deficiency in BABA-IR against Pst DC3000. Absence of PR-1 (PATHOGENESIS-RELATED 1) potentiation was correlated with this deficiency even though the lecRK-a1 mutant still responded normally towards other virulent and avirulent pathogens. We conclude that this lectin receptor kinase is necessary for BABA-IR and BABA-mediated priming of Arabidopsis defense responses towards virulent bacteria. Since LecRK-a1 is induced early during infection, it may be involved in plant-microbe recognition. |
URI: | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/26748 |
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顯示於系所單位: | 植物科學研究所 |
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