翟 浩，李曉軍，余賢美，王海波，馬亞男

(山東省果樹(shù)研究所，山東泰安 271000)

植物真菌病害可造成巨大的產(chǎn)量損失，且一直威脅全球的食品安全[1-2]。培育和種植抗病品種是控制植物真菌病害較為有效且環(huán)保的方法[3]。目前，從分子和遺傳學(xué)角度對(duì)植物病原真菌進(jìn)行了較為深入的研究，揭示了大量真菌的分子致病機(jī)理[4-5]。

蘋(píng)果炭疽葉枯病(Glomerellaleaf spot,GLS)是由刺盤(pán)孢屬(Colletotrichum)真菌引起的蘋(píng)果部分栽培品種的葉部病害，近年來(lái)該病害在我國(guó)各蘋(píng)果產(chǎn)區(qū)普遍發(fā)生，可造成蘋(píng)果樹(shù)葉片大量脫落和果實(shí)腐爛，進(jìn)而削弱樹(shù)勢(shì)，引起次年果實(shí)減產(chǎn)甚至絕產(chǎn)，嚴(yán)重制約了蘋(píng)果產(chǎn)業(yè)的健康可持續(xù)發(fā)展[6]。深入研究蘋(píng)果炭疽葉枯病菌的分子致病機(jī)理，有助于分析蘋(píng)果炭疽葉枯病發(fā)展迅速、危害嚴(yán)重的原因，為針對(duì)該病害的藥劑研發(fā)和果園管理措施優(yōu)化提供參考，同時(shí)為研究其他病原菌與植物的互作機(jī)制提供理論依據(jù)。

1 蘋(píng)果炭疽葉枯病研究現(xiàn)狀

蘋(píng)果炭疽葉枯病是我國(guó)近年來(lái)新發(fā)現(xiàn)的一種流行性病害，主要危害嘎啦和金冠系列蘋(píng)果品種。Wang 等[7]對(duì)我國(guó)蘋(píng)果炭疽葉枯病的癥狀和病原進(jìn)行了首次報(bào)道。目前，該病害逐漸蔓延，在山東、陜西、遼寧、河南和河北等主要蘋(píng)果生產(chǎn)省份已普遍發(fā)生[6]。

蘋(píng)果炭疽葉枯病最初被認(rèn)為由圍小叢殼(Glomerellacingulata,無(wú)性態(tài)為膠孢炭疽菌C.gloeosporioides)引起[8]。后經(jīng)研究發(fā)現(xiàn)，尖胞炭疽菌(C.acutatum)[9]和喀斯特炭疽菌(C.karstii)[10]也可引起蘋(píng)果炭疽葉枯病。王薇等[11]根據(jù)新的刺盤(pán)孢分類(lèi)系統(tǒng)[12]，利用形態(tài)學(xué)、培養(yǎng)特性、多基因系統(tǒng)發(fā)育及致病性等特征，明確了河南省和陜西省部分蘋(píng)果產(chǎn)區(qū)蘋(píng)果炭疽葉枯病的病原為果生刺盤(pán)孢(C.fructicola)和隱秘刺盤(pán)孢(C.aenigma)2種。通過(guò)對(duì)山東省蘋(píng)果主產(chǎn)區(qū)蘋(píng)果炭疽葉枯病病原的形態(tài)學(xué)研究和多基因系統(tǒng)發(fā)育分析，認(rèn)為引起該地區(qū)蘋(píng)果炭疽葉枯病的病原為果生刺盤(pán)孢(C.fructicola)。

近年來(lái)，國(guó)內(nèi)外對(duì)于蘋(píng)果炭疽葉枯病的研究集中于病原群體結(jié)構(gòu)、病原侵染機(jī)制、病害發(fā)生規(guī)律和藥劑防治等。符丹丹等[13]利用優(yōu)化后的ISSR-PCR反應(yīng)體系對(duì)蘋(píng)果炭疽葉枯病菌遺傳多樣性進(jìn)行分析。任斌等[14]利用光學(xué)顯微鏡和掃描電鏡對(duì)圍小叢殼(G.cingulata)在嘎啦蘋(píng)果葉片上的侵染過(guò)程進(jìn)行了研究，認(rèn)為該菌發(fā)育和侵染過(guò)程中的一些特點(diǎn)可能是造成病害暴發(fā)的原因。王冰等[15-16]檢測(cè)了6種藥劑對(duì)圍小叢殼的內(nèi)吸治療效果和8種藥劑的保護(hù)效果，并測(cè)試了溫度、濕度和光照對(duì)該菌產(chǎn)生分生孢子和子囊孢子的影響。王海艷等[17]和張俊祥等[18]建立并優(yōu)化了農(nóng)桿菌介導(dǎo)的圍小叢殼的遺傳轉(zhuǎn)化體系，吳建圓等[19]利用農(nóng)桿菌介導(dǎo)的轉(zhuǎn)化技術(shù)將nptⅡ(新霉素磷酸轉(zhuǎn)移酶基因)基因盒整合到圍小叢殼基因組中，韓小路等[20]建立了聚乙二醇介導(dǎo)的果生刺盤(pán)孢(C.fructicola)原生質(zhì)體的轉(zhuǎn)化體系。

目前，從分子角度對(duì)蘋(píng)果炭疽葉枯病菌與寄主互作機(jī)制的研究相對(duì)較少。Perfect等[21]認(rèn)為刺盤(pán)孢屬(Colletotrichum)真菌是研究植物病原真菌與寄主互作非常理想的模式菌之一。Sygmund等[22-23]對(duì)圍小叢殼的一個(gè)依賴(lài)于FAD的葡萄糖脫氫酶基因進(jìn)行了真核和原核表達(dá)，該酶被認(rèn)為可以抑制植物漆酶、酚氧化酶和過(guò)氧化氫酶的活性，在侵染植物過(guò)程中可能起促進(jìn)作用。Seman等[24]利用畢赤酵母對(duì)圍小叢殼的角質(zhì)酶基因進(jìn)行了高效表達(dá)。Wang等[25-26]研究認(rèn)為，茉莉酸、脫落酸和一些芳香揮發(fā)物的協(xié)同作用在葡萄果實(shí)抵御圍小叢殼的侵染過(guò)程中發(fā)揮著重要作用。Velho等[27]研究發(fā)現(xiàn)果生刺盤(pán)孢可以通過(guò)抑制植物的氧化防衛(wèi)反應(yīng)來(lái)達(dá)到在蘋(píng)果葉片上成功定殖和侵染的目的。雖然這些研究均為蘋(píng)果炭疽葉枯病菌的研究奠定了一定基礎(chǔ)，但對(duì)于蘋(píng)果炭疽葉枯病菌-蘋(píng)果葉片這個(gè)病害系統(tǒng)，病原表達(dá)在互作過(guò)程中發(fā)揮關(guān)鍵作用的蛋白質(zhì)分子尚未做出明確判斷和功能驗(yàn)證。因此，從互作蛋白著手，探討蘋(píng)果炭疽葉枯病的分子致病機(jī)理，從根本上解析該病害發(fā)展迅速、危害嚴(yán)重的原因是十分必要的。

2 植物的先天免疫系統(tǒng)與互作蛋白

植物的先天免疫反應(yīng)包含2個(gè)層面[28]，其中第1個(gè)層面是由病原相關(guān)分子模式(pathogen-associated molecular patterns，PAMPs)觸發(fā)的免疫反應(yīng)(PAMPs triggered immunity，PTI)。PTI通過(guò)植物跨膜的模式識(shí)別受體(pattern-recognition receptors，PRRs)來(lái)實(shí)現(xiàn)，PRRs可以識(shí)別保守的病原相關(guān)分子模式，激活寄主植物的第一層免疫反應(yīng)來(lái)抵御入侵微生物的定殖[3,29-30]。植物的PRRs感知PAMPs，會(huì)快速啟動(dòng)與PTI相關(guān)的一系列反應(yīng)，包括絲裂原活性蛋白的級(jí)聯(lián)、防衛(wèi)反應(yīng)相關(guān)基因的響應(yīng)和細(xì)胞死亡等[5,31-32]。植物先天免疫系統(tǒng)的第2個(gè)層面是以高度多樣化的抗性蛋白(R蛋白)為基礎(chǔ)，這些R蛋白可以識(shí)別各種病原效應(yīng)蛋白(effector)，激活植物的免疫反應(yīng)，即蛋白觸發(fā)的免疫反應(yīng)(effector-triggered immunity，ETI)[33-34]。ETI大多在細(xì)胞內(nèi)進(jìn)行，往往十分迅速和強(qiáng)烈，常會(huì)伴隨著植物的過(guò)敏性壞死反應(yīng)(hypersensitive reaction,HR)[3]。不同種類(lèi)炭疽菌的體外基因敲出和回補(bǔ)課題的開(kāi)展促進(jìn)了對(duì)這類(lèi)模式病原物的研究和利用[21]，目前已對(duì)可侵染模式植物擬南芥(Arabidopsisthaliana)和十字花科蔬菜的菜炭疽菌(C.higginsianum)[35-37]和可侵染本氏煙(Nicotianabenthamiana)和煙草(N.tabacum)以及西瓜炭疽菌(C.orbiculare)[38]進(jìn)行了深入研究。然而，對(duì)重要經(jīng)濟(jì)作物炭疽病菌的PAMPs和效應(yīng)蛋白的研究，還遠(yuǎn)滯后于對(duì)這些真菌的次生代謝分析等生物化學(xué)方面，到目前為止僅少數(shù)幾種效應(yīng)蛋白得到驗(yàn)證[39-42]。

PAMPs能在植物組織表面、植物細(xì)胞間隙或植物細(xì)胞內(nèi)起作用[43-44]，通過(guò)與寄主細(xì)胞的靶蛋白結(jié)合，刺激植物快速產(chǎn)生Ca2+、NO和H2O2等早期免疫防御反應(yīng)信號(hào)分子[45]，這些信號(hào)分子通過(guò)復(fù)雜的信號(hào)網(wǎng)絡(luò)進(jìn)行逐級(jí)傳遞放大，產(chǎn)生乙烯、水楊酸、吲哚乙酸、茉莉酸、植保素和病程相關(guān)蛋白等，最終使植物獲得系統(tǒng)抗病性[46]。PAMPs與植物靶蛋白的結(jié)合在誘導(dǎo)植物抗病信號(hào)轉(zhuǎn)導(dǎo)途徑中發(fā)揮著重要作用，是揭示激發(fā)子誘導(dǎo)植物抗病分子機(jī)制的關(guān)鍵環(huán)節(jié)。研究發(fā)現(xiàn)，植物病原真菌的一個(gè)內(nèi)切纖維素酶，具有PAMPs功能，可以誘導(dǎo)植物的防衛(wèi)反應(yīng)(植物細(xì)胞過(guò)敏性壞死反應(yīng)、植物防衛(wèi)反應(yīng)基因表達(dá)、活性氧產(chǎn)生、培養(yǎng)基堿化、鈣離子積累、乙烯合成等)，并其激發(fā)活性與催化活性不相關(guān)[32]。具有激發(fā)子功能的真菌木聚糖酶、果膠酶和內(nèi)切纖維素酶等被稱(chēng)為PAMPs分子[5,47-49]。PAMPs涉及各種結(jié)構(gòu)的分子，并在病原種屬間保守。較為典型的PAMPs有細(xì)菌中的鞭毛蛋白、延伸因子EF-Tu、肽聚糖和脂多糖等，真菌中有細(xì)胞壁多聚糖和幾丁質(zhì)等，卵菌中有葡聚糖[50-52]。一般認(rèn)為PAMPs在微生物適應(yīng)與生存過(guò)程中發(fā)揮重要作用[53]。

效應(yīng)蛋白方面，目前研究證實(shí)可以利用病原效應(yīng)蛋白作為分子探針，篩選鑒定寄主的感病基因(S基因)[54]。感病基因編碼蛋白被病原真菌識(shí)別，引起病原菌擴(kuò)散并最終導(dǎo)致植物組織病害。如果使植物感病基因失活，則可以降低病原菌的致病能力，誘導(dǎo)寄主產(chǎn)生持久的抗病性[55]。近10年來(lái)，多項(xiàng)研究也證實(shí)了這一點(diǎn)，以植物感病基因?qū)Σ≡婢?yīng)蛋白的識(shí)別為基礎(chǔ)產(chǎn)生的免疫反應(yīng)，可以抵御多種病原菌的侵染[54]。

包括蘋(píng)果炭疽葉枯病菌在內(nèi)的植物病原真菌都會(huì)在侵染寄主過(guò)程中表達(dá)分泌互作蛋白，尤其是PAMPa和效應(yīng)蛋白。期望通過(guò)對(duì)蘋(píng)果炭疽葉枯病菌-蘋(píng)果葉片這個(gè)病害系統(tǒng)中互作蛋白的篩選與功能驗(yàn)證，尋找保守的PAMPs和效應(yīng)蛋白分子，分析和討論蘋(píng)果炭疽葉枯病菌的分子致病機(jī)理。

3 展望

我國(guó)是世界蘋(píng)果生產(chǎn)大國(guó)，種植面積和產(chǎn)量均居世界前列。近年來(lái)，蘋(píng)果炭疽葉枯病在全國(guó)各蘋(píng)果產(chǎn)區(qū)大范圍暴發(fā)，嚴(yán)重影響了果實(shí)的產(chǎn)量和品質(zhì)，制約了蘋(píng)果產(chǎn)業(yè)的健康可持續(xù)發(fā)展。目前對(duì)蘋(píng)果炭疽葉枯病菌分子致病機(jī)理和蘋(píng)果抗病機(jī)理的研究尚不充分。以蘋(píng)果炭疽葉枯病菌為研究對(duì)象，從病原-寄主互作蛋白著手，闡述該病菌的分子致病機(jī)理，可以為防控藥劑研發(fā)和管理措施優(yōu)化提供參考，為該病害防治及抗病品種培育提供新思路。

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