科學(xué)家的一項(xiàng)最新研究確定了植物免疫響應(yīng)過程中的一個(gè)關(guān)鍵信號(hào)——水楊酸甲酯（methyl salicylate），這種類似阿司匹林的物質(zhì)能夠提升植物免疫系統(tǒng)的“警戒等級(jí)”,。該研究成果有望使科學(xué)家改造植物的防御能力,，相關(guān)論文發(fā)表在10月5日的《科學(xué)》雜志上,。
盡管植物并沒有人類的T細(xì)胞或者其他免疫功能細(xì)胞，但早在100多年前,，科學(xué)家就知道植物也會(huì)通過某種信號(hào)途徑來引發(fā)整個(gè)植物體的免疫抵抗,。這種作用被稱為系統(tǒng)獲得抗病性（systemic acquired resistance），植物被入侵部分發(fā)出的信號(hào)會(huì)傳播到其他未被感染的部分,。
論文高級(jí)作者,、美國康奈爾大學(xué)植物研究所的Daniel F. Klessig表示，利用新的發(fā)現(xiàn),，科學(xué)家可以通過基因技術(shù)改變?cè)撔盘?hào)途徑,，從而提升植物的自身防御能力，提高作物產(chǎn)量,，并減少殺蟲劑的使用,。
1990年，Klessig的小組報(bào)告說,，水楊酸和一氧化氮是植物中兩種關(guān)鍵的防御信號(hào)路徑,。2003年和2005年，該小組在《美國國家科學(xué)院院刊》上發(fā)表文章稱,，一種名為SABP2的蛋白酶是植物系統(tǒng)獲得抗病性所必需的,，它能夠使水楊酸甲酯轉(zhuǎn)化成水楊酸,。
在這些研究中,，Klessig等人發(fā)現(xiàn)，植物受到病原體攻擊后,，它們?cè)诟腥静课恢圃斐鏊畻钏醽砑せ罘烙鶛C(jī)制,。其中一些水楊酸會(huì)轉(zhuǎn)化成水楊酸甲酯，后者通過SABP2蛋白重新形成水楊酸,。此外,，研究還表明，在未被感染的植物葉子中,，SABP2必須十分活躍,，才能導(dǎo)致系統(tǒng)獲得抗病性完全形成。與之相比,，在被感染的葉子中,，SABP2必須通過與水楊酸結(jié)合，從而使活性受到抑制,。
“正是這種滅活作用產(chǎn)生了水楊酸甲酯”,，Klessig說，“它通過導(dǎo)管到達(dá)未感染組織,，通過SABP2重新形成水楊酸,，打開該部位的防御機(jī)制,。”
盡管這項(xiàng)新的研究意義重大，但科學(xué)家仍對(duì)一個(gè)問題迷惑不解,，那就是為何植物要如此麻煩地將水楊酸甲酯傳輸?shù)轿锤腥镜慕M織,，而不直接傳輸水楊酸。（科學(xué)網(wǎng) 任霄鵬/編譯）
原始出處:
Science 5 October 2007:
Vol. 318. no. 5847, pp. 113 - 116
DOI: 10.1126/science.1147113
Methyl Salicylate Is a Critical Mobile Signal for Plant Systemic Acquired Resistance
Sang-Wook Park, Evans Kaimoyo, Dhirendra Kumar,* Stephen Mosher, Daniel F. Klessig
In plants, the mobile signal for systemic acquired resistance (SAR), an organism-wide state of enhanced defense to subsequent infections, has been elusive. By stimulating immune responses in mosaic tobacco plants created by grafting different genetic backgrounds, we showed that the methyl salicylate (MeSA) esterase activity of salicylic acid–binding protein 2 (SABP2), which converts MeSA into salicylic acid (SA), is required for SAR signal perception in systemic tissue, the tissue that does not receive the primary (initial) infection. Moreover, in plants expressing mutant SABP2 with unregulated MeSA esterase activity in SAR signal–generating, primary infected leaves, SAR was compromised and the associated increase in MeSA levels was suppressed in primary infected leaves, their phloem exudates, and systemic leaves. SAR was also blocked when SA methyl transferase (which converts SA to MeSA) was silenced in primary infected leaves, and MeSA treatment of lower leaves induced SAR in upper untreated leaves. Therefore, we conclude that MeSA is a SAR signal in tobacco.
Boyce Thompson Institute for Plant Research, Tower Road, Ithaca, NY 14853, USA.
* Present address: Department of Biological Sciences, East Tennessee State University, Johnson City, TN 37614, USA.
Present address: Department of Cell and Systems Biology, University of Toronto, Toronto, Ontario M5S 3B2, Canada.
To whom correspondence should be addressed. E-mail: [email protected]
