曠永潔 柳浪 嚴芳 任斌, 閆大琦 張大偉 林宏輝 周煥斌
(1. 中國農(nóng)業(yè)科學院植物保護研究所 植物病蟲害生物學國家重點實驗室,北京 100193;2. 四川大學生命科學學院 生物資源與生態(tài)環(huán)境教育部重點實驗室,成都 610065)
水稻作為一種主要糧食作物,養(yǎng)活了世界上一半以上的人口,預(yù)計到2050年世界人口將增加到90億左右,而水稻產(chǎn)量至少需要翻一番[1-2]。但是在水稻生產(chǎn)過程中,稻瘟病、稻曲病、紋枯病、白葉枯病、細菌性條斑病和黑條矮縮病等病害,嚴重危害著水稻的生長發(fā)育,進而造成了極大的產(chǎn)量損失和品質(zhì)降低,威脅著全球的糧食安全。
為了抵御各種病原物的感染,植物已經(jīng)進化出復(fù)雜的防御系統(tǒng),其主要由各種信號轉(zhuǎn)導(dǎo)途徑組成的復(fù)雜分子網(wǎng)絡(luò)所構(gòu)成,其中植物激素及其信號轉(zhuǎn)導(dǎo)網(wǎng)絡(luò)占據(jù)著重要的地位[3-5]。大量研究表明,水楊酸(Salicylates,SAs)、茉莉酸(Jasmonates,JAs)和乙烯(Ethylene,ET)在植物與病原物互作過程中發(fā)揮了關(guān)鍵的作用;油菜素內(nèi)酯(Brassinosteroids,BRs)、赤霉素(Gibberellins,GAs)、脫落酸(Abscisic acid,ABA)、生長素(Auxin,IAA)和細胞分裂素(Cytokinins,CKs)等植物生長發(fā)育相關(guān)的激素也直接或間接地參與了植物抗病或感病反應(yīng)。不同的植物激素信號通路在植物和病原物互作中行使不同的功能,且各通路之間相互關(guān)聯(lián),相互影響,協(xié)同調(diào)控著植物的生長發(fā)育以及對外防御反應(yīng),使植物無時不處在一種生理平衡之中,最大程度地保護自身。另一方面,植物病原菌入侵植物時,通過分泌多種效應(yīng)蛋白、或直接分泌激素或激素類似物至植物細胞內(nèi),干擾植物激素的合成、代謝及其信號分子網(wǎng)絡(luò),減弱植物的抗病防御反應(yīng),達到致病目的。效應(yīng)蛋白與激素網(wǎng)絡(luò)的互作,在一定程度上決定了病原菌與寄主植物在斗爭時的此消彼長。
擬南芥一直是解析植物病原物互作中植物激素分子信號網(wǎng)絡(luò)的模式植物。然而,愈來愈多的證據(jù)表明,作為單子葉農(nóng)作物的模式植物,水稻有著其獨特的一面,其對于指導(dǎo)水稻、小麥、大麥、玉米等農(nóng)作物的生產(chǎn)育種有著重要意義。尤其是最新開發(fā)的基因組定點編輯技術(shù),利用其對激素信號通路關(guān)鍵基因的改造,直接進行分子育種,對現(xiàn)代水稻農(nóng)業(yè)生產(chǎn)具有極大的推動作用。因此,本文從以上提到的幾種植物激素出發(fā),論述它們及其涉及的信號組分在水稻與病原物互作中的作用,為下一步的研究發(fā)展和生產(chǎn)應(yīng)用提供理論依據(jù)。
White等[5-7]在煙草中首次發(fā)現(xiàn)了SA在植物抗病中的作用。此后,SA與植物抗病性的關(guān)系逐漸得到研究者的廣泛重視,目前研究表明SA參與擬南芥、煙草、水稻等多種植物的抗病性。SA是一類簡單的酚類化合物,在植物的防御系統(tǒng)中具有重要作用,尤其是系統(tǒng)獲得性抗性(Systemic acquired resistance,SAR)。在受到病原物侵染后,植物體內(nèi)的SA大量積累,導(dǎo)致病程相關(guān)蛋白(Pathogenesisrelated proteins,PRs)的表達,增加了植物對病原菌侵染的抗性[8-10]。
水稻植株內(nèi)源基礎(chǔ)SA含量較高(5 000-30 000 ng/g 植株鮮重),甚至高于受侵染的擬南芥、煙草等植物組織,高含量的SA可以作為一個內(nèi)源抗氧化劑,保護水稻免受由老化、病原菌侵染及非生物脅迫帶來的損傷[11-15]。Isochorismate synthase(ICS)和Phenylalanine ammonialyase(PAL)基因的同源基因負責水稻植株內(nèi)SA的合成[16-18],其中,ICS途徑被認為是持續(xù)合成SA的主要來源,而PAL途徑僅僅只是在局部壞死的細胞內(nèi)快速的形成SA[9,19]。當水稻被線蟲(Meloidogyne graminicola和Hirschmanniella oryzae)侵染后,OsICS在植株體內(nèi)不同部位不同時期內(nèi)的表達均顯著下調(diào),而OsPAL則在線蟲侵染部位顯著上調(diào),在其他部位則表達不明顯或者出現(xiàn)下調(diào)[20],但這并不能排除PAL途徑對合成SA的重要性。SA參與植物對生物和非生物脅迫響應(yīng)過程,明確其合成途徑的關(guān)鍵酶及其合成機制非常重要。
SA途徑的主調(diào)控蛋白NPR1位于SA生物合成的下游,PRs基因上游。過表達OsNPR1或其同源基因,能增加水稻抗病性[21-27]。核內(nèi)NPR1的表達水平對于植物誘導(dǎo)抗病至關(guān)重要,當植物缺失OsNPR1時,會導(dǎo)致SA誘導(dǎo)的轉(zhuǎn)錄缺陷,不能激活SAR反應(yīng)。在沒有病原物侵染時,NPR1蛋白的C端轉(zhuǎn)錄激活結(jié)構(gòu)域被其N端BTB/POZ結(jié)構(gòu)域抑制,使NPR1處于失活狀態(tài),而SA的存在使NPR1蛋白構(gòu)像發(fā)生改變,解除自身抑制作用,激活NPR1[28-29]。在擬南芥中,NPR1及其同源蛋白NPR3、NPR4都具有結(jié)合SA的能力,但NPR1只在合適的平衡溶液中才能結(jié)合SA[30-33]。NPR3和NPR4都能直接結(jié)合SA,但是NPR3結(jié)合親和力較NPR4弱。在SA濃度低時,SA與NPR4結(jié)合,通過26S蛋白酶體降解NPR1,而當病原物侵染誘導(dǎo)SA濃度增加時,NPR3被激活并結(jié)合SA形成NPR3-SA復(fù)合體,促進NPR1的降解。只有當SA處于合適濃度時,才能實現(xiàn)NPR1蛋白的積累,從而激活SA介導(dǎo)的轉(zhuǎn)錄活性,調(diào)控植物防御反應(yīng)[32-36]。NPR1、NPR3和NPR4相互作用,形成植株感受并傳遞SA信號的模型。但是目前影響NPRs與SA結(jié)合能力的因素暫不清楚。
除NPR1之外,水稻中SA信號途徑還含有一個主調(diào)控因子WRKY45,當用SA類似物Benzothiadiazole(BTH)處理水稻植株3 h后,OsWRKY45基因表達上調(diào),過表達OsWRKY45可顯著增強水稻 對 稻 瘟 病 菌Magnaporthe oryzae的 抗 性[37-41]。OsWRKY45基因在水稻粳稻(OsWRKY45-1)和秈稻(OsWRKY45-2)中存在序列差異,OsWRKY45-1在第一個內(nèi)含子序列中存在一個含osa-miR815b的502 個核苷酸的插入,這也導(dǎo)致了兩個WRKY45等位基因發(fā)揮著不同的作用[42]。過表達OsWRKY45-1的植株,其接種水稻白葉枯病菌Xanthomonas oryzaepv.oyrzae(Xoo)后病斑面積比野生型高10%以上,增加了植株感病性;而過表達OsWRKY45-2的植株則與之相反,病斑面積減少了30%以上[43]。OsWRKY45兩個等位基因在對ABA的敏感度,鹽脅迫也呈相反的響應(yīng),但是對干旱和低溫脅迫則表現(xiàn)出相似的響應(yīng)[44]。2016年研究發(fā)現(xiàn),來源于OsWRKY45-1的osamiR815b(TE-siR815b)是造成這種現(xiàn)象的主要原因[42]。在水稻受到Xoo侵染后,在含OsWRKY45-1的 品 種 Dongjin中 osa-miR815b(TE-siR815b) 的積累增加,而含OsWRKY45-2的品種Minghui 63則無顯著變化。同時在過表達OsWRKY45-1的植株(WRKY45-1-oe) 中,TE-siR815b和OsWRKY45-1的轉(zhuǎn)錄顯著增加,而在過表達OsWRKY45-2的植株(WRKY45-2-oe)中,只有OsWRKY45-2的轉(zhuǎn)錄顯著增加,說明TE-siR815b的表達與OsWRKY45-1激活表達相關(guān)。含有W-box或類似于W-box序列的siR815 Target 1(ST1)是 TE-siR815b的靶標基因,該基因在WRKY45-1-oe中的表達被抑制,而在WRKY45-2-oe中的表達卻被激活,且WRKY45-1-oe中的ST1的DNA甲基化水平顯著高于WRKY45-2-oe中,ST1的表達并不依賴于TE-siR815b。結(jié)果揭示了TE-siR815b通過增加ST1DNA甲基化的水平,抑制了ST1的表達,進而導(dǎo)致了OsWRKY45在不同品種水稻的防御反應(yīng)中具有不同作用。OsWRKY45受到MAPKs的調(diào)節(jié)作用。MAPKs偏好利用Ser/Thr-Pro作為其磷酸化靶標位點,而WRKY45含有3個作用位點。研究發(fā)現(xiàn)OsMPK4和OsMPK6可以在離體條件下磷酸化WRKY45蛋白,而且在SA處理后水稻細胞中OsMPK6活性迅速提高,磷酸化并激活WRKY45蛋白以應(yīng)對病原侵染。Ser294和Ser299磷酸化負責激活OsWRKY45,而Thr266磷酸化則負調(diào)控OsWRKY45介導(dǎo)的抗病性[45-47]。這種激活效應(yīng)會被由ABA調(diào)控的OsPTP1/2抑制[46]。此外,細胞核內(nèi)OsWRKY45的降解也受到泛素蛋白酶系統(tǒng)(Ubiquitin proteasome system,UPS)調(diào)控[48]。其它WRKYs基因也參與調(diào)控水稻對病原物的抗病反應(yīng),如OsWRKY42、OsWRKY51、OsWRKY68、OsWRKY13和OsWRKY62等[49-53]。
研究人員發(fā)現(xiàn),在擬南芥中WRKYs基因受到OsNPR1基因的調(diào)控,與之不同的是,在BTH誘導(dǎo)的防御反應(yīng)中,水稻中OsNPR1和OsWRKY45是兩個獨立的調(diào)控途徑[37-41],但這也并不表明OsNPR1和OsWRKY45是兩個絕對獨立的途徑。據(jù)報道,OsDjA6的RNAi植株能夠顯著增加水稻對M. oryzae的防御能力,且RNAi植株中OsWRKY45、OsNPR1和OsPR5的RNA水平是野生型TG394的2-4倍。同時用flg22和Chitin處理OsDjA6的RNAi植株發(fā)現(xiàn),RNAi植株中活性氧(Reactive oxygen species,ROS)積累顯著增加,結(jié)果表明OsDjA6作為負調(diào)控因子調(diào)控水稻PTI(PRR-triggered immunity)和SA途徑[54]。這也說明在其上游可能存在能同時調(diào)控它們的基因,但仍需要進一步的研究證實。
JA及其衍生物存在于多種高等植物,參與調(diào)節(jié)植物的生長發(fā)育和植物免疫反應(yīng)[55]。在擬南芥中,JA能夠增強對死體營養(yǎng)型病原物的抗性;相反,對活體營養(yǎng)型病原物的敏感性增強,抗性減弱[56-59]。丁香假單胞菌Pseudomonas syringae侵染時,通過向細胞內(nèi)分泌JA類似物—coronatine毒素,去干擾寄主植物的激素信號通路,達到致病的目的[60]。JA途徑通過調(diào)節(jié)活性效應(yīng)物JA-Ile、JA受體復(fù)合物SCFCOI1、JA轉(zhuǎn)錄抑制子JAZ蛋白、JA途徑主要轉(zhuǎn)錄因子MYC2、JA衍生物MeJA、JA合成相關(guān)基因AOC和WRKY等其他信號通路轉(zhuǎn)錄因子之間的相互作用來調(diào)控植物防御反應(yīng)[61-67]。
JA能夠從多方面增強水稻對植物病原真菌、細菌和病毒的抗性。如外源噴施JA能增強水稻對黃單胞桿菌Xanthomonas oryzae的抗性[68],還能增強小麥對白粉病的抗性[69-70];JA通過苯丙氨酸途徑誘導(dǎo)水稻對立枯絲核菌Rhizoctonia solani的抗性,外源噴施JA 5 d后,選擇完整的葉鞘接種R. solani,接種4 d后發(fā)現(xiàn)JA處理的植株能夠形成木質(zhì)素以抑制病原菌擴展[71];此外,葉面噴施茉莉酸甲酯(MeJA)降低了水稻黑條矮縮?。≧ice black-streaked dwarf virus,RBSDV)的發(fā)病率,證實JA能夠增加水稻對RBSDV的抗性[72]。與野生型相比,JA合成途徑基因OsAOC缺失突變體對M. oryzae抗性降低,表現(xiàn)為菌絲生長更快且JA含量降低,揭示OsAOC能通過JA信號途徑調(diào)控水稻對M. oryzae的免疫反應(yīng)[73];另一方面,過表達OsWRKY30可誘導(dǎo)JA途徑中OsLOX,OsAOS2表達,同時伴隨內(nèi)源JA積累,對M. oryzae和R. solani的抗性增強[74]。
在擬南芥中,當受到病原物侵染時,JA水平上升,在活性信號分子JA-Ile的作用下,COI1與JAZ蛋白結(jié)合,在泛素連接酶復(fù)合體(SCFCOI1)的作用下使JAZ蛋白泛素化并通過26S蛋白酶體途徑被降解,JAZ蛋白對轉(zhuǎn)錄因子或信號轉(zhuǎn)導(dǎo)蛋白的抑制作用被解除,從而激活JA調(diào)控的防御反應(yīng)[75-76]。在水稻中,通過酵母雙雜交試驗發(fā)現(xiàn)水稻OsCOIs與OsJAZs存在相互作用,且過表達OsCOI1a或OsCOI1b可恢復(fù)擬南芥coi1-1突變體中被抑制的JA信號[77]。此外,外源JA顯著上調(diào)JAZ8表達,通過SCFCOI1E3泛素連接酶復(fù)合體降解JAZ8,增強水稻對Xoo的抗性,JAZ8作為JA途徑的防御抑制子負調(diào)節(jié)JA誘導(dǎo)的水稻對Xoo的抗性[78],隨后的研究表明JAZ通過調(diào)節(jié)芳樟醇的合成來進一步調(diào)控水稻對Xoo的抗性[55]。OsMYC2作為早期JA信號的正調(diào)控因子,能夠與OsJAZ10的啟動子結(jié)合激活JA途徑,OsMYC2過表達植株表現(xiàn)出對Xoo更強的抗病性,RNA-seq分析表明在OsMYC2RNAi突變體中,依賴于JA途徑的抗病基因、JA合成基因表達量顯著下降,這些結(jié)果顯示OsMYC2在JA調(diào)控水稻抗病過程中具有重要作用[79-80]。但是要解析JA的合成及調(diào)控途徑在水稻抗病性中的作用機制,還有待進一步研究。
ET是植物體內(nèi)的一種重要氣態(tài)激素,主要調(diào)控種子的萌發(fā)和生長、葉片和組織的衰老、果實的成熟等植物生長發(fā)育過程,在植物響應(yīng)生物和非生物脅迫中也具重要作用。大量研究表明乙烯參與調(diào)控擬南芥、煙草、番茄、水稻和大豆等多種植物的免疫反應(yīng)。在植物免疫反應(yīng)中,乙烯通常被認為是和JA一起協(xié)同參與誘導(dǎo)植物對死體營養(yǎng)型病原菌的抗性,而拮抗SA介導(dǎo)的對活體營養(yǎng)型病原菌的抗性[81]。
在M. oryzae侵染水稻過程中,與感病材料相比,抗病材料中乙烯信號途徑被激活,乙烯積累量顯著提高;乙烯合成抑制劑氨基氧乙酸(Aminooxyacetic acid,AOA)和受體結(jié)合抑制劑1-甲基環(huán)丙烯(1-methylcyclopropene,1-MCP)處理可顯著降低寄主的抗病性[82-83]。進一步研究顯示,在水稻抗稻瘟病的過程中,乙烯信號下游轉(zhuǎn)錄因子OsEIL1可激活OsrbohA/OsrbohB和OsOPRs基因表達,繼而激活ROS迸發(fā)和植保素積累[83]。而將乙烯信號的中心傳遞者OsEIN2b沉默后,增加了水稻對稻瘟病的感病性,表現(xiàn)為病原菌生長更快[84]。乙烯也參與調(diào)控水稻系統(tǒng)獲得性抗性。葉片噴施乙烯利可誘導(dǎo)激活水稻根部的PRs基因和JA信號響應(yīng)基因OsJAmyb表達,接種實驗證實其對根結(jié)線蟲抗性顯著提高;OsEIN2bRNAi突變體也比野生型更感病,且乙烯利處理并不能恢復(fù)其表型;AOA處理也能降低水稻抗病性,即乙烯信號傳導(dǎo)參與了乙烯誘導(dǎo)的對根結(jié)線蟲系統(tǒng)獲得性抗性[85]。
此外,乙烯的合成在水稻抗病反應(yīng)中也具有非常重要的作用。Helliwell等[86]發(fā)現(xiàn)過表達乙烯生物合成限速酶基因OsACS2后,水稻對M. oryzae和R.solani的抗性顯著增強。在過表達水稻抗稻瘟病蛋白Pik-H4的互作蛋白OsBIHD1植株中,OsBIHD1結(jié)合在OsACO3的啟動子區(qū)域激活OsACO3,促進OsACOs表達,這表明乙烯合成在OsBIHD1正調(diào)控水稻抗病反應(yīng)中具有重要作用[87]。
也有研究表明乙烯可負調(diào)控水稻免疫反應(yīng)。如外源噴施乙烯利會增加水稻對Cochliobolus miyabeanus的感病性[88],而這種負調(diào)控作用能夠被硅處理抑制[89]。Shen等[90-91]發(fā)現(xiàn)水稻OsEDR1(Enhanced disease resistance 1)基因敲除突變體表現(xiàn)出對Xoo明顯的抗性,在OsEDR1敲除突變體中乙烯合成基因ACSs家族的5個基因表達均受到抑制且乙烯的含量也降低,而乙烯合成前體ACC處理可抑制OsEDR1敲除突變對Xoo的抗性。結(jié)果表明OsEDR1基因介導(dǎo)乙烯負調(diào)控水稻對Xoo的防御反應(yīng),同時促進ET的合成,抑制SA和JA相關(guān)的防御反應(yīng)。
和擬南芥一樣,乙烯在水稻抗病過程中既可作為正調(diào)控因子也可是負調(diào)控因子,這種調(diào)節(jié)作用可能取決于植物-病原菌之間的互作模式及特定的環(huán)境條件[92-93]。
BR是調(diào)控植物生長和發(fā)育的一類重要的類甾醇激素,在植物全生育期均具有廣泛的生理作用。而近年來研究發(fā)現(xiàn),BR在植物應(yīng)答非生物和生物脅迫反應(yīng)中也具有非常重要的作用。BR受體BRI1在識別結(jié)合BR后與其共受體BAK1形成異源二聚體,激活二者激酶活性并通過一系列磷酸化作用將信號傳遞至負調(diào)控因子GSK3類激酶 BIN2,解除BIN2對轉(zhuǎn)錄因子BZR1 和BES1磷酸化;去磷酸化的BZR1和BES1可進入細胞核并調(diào)控BR響應(yīng)基因表達[94]。BR和PTI信號通路間存在許多共同組分,如BAK1、BSK1和BIK1等,而且PTI途徑中的FLS2感知flg22后的也需要和BAK1形成異源二聚體并激活下游信號途徑[95-96]。這些相似之處暗示著BR和PTI信號之間可能存在交聯(lián)互作,即BR也可能參與植物免疫反應(yīng)。
早在 2003年,Nakashita等[97]研究發(fā)現(xiàn)BR處理可減輕水稻稻瘟病和白葉枯病癥狀。此外,OsSERK2可正調(diào)控類受體激酶Xa21介導(dǎo)的免疫反應(yīng),降低OsSERK2表達量可抑制Xa21介導(dǎo)的水稻對Xoo的抗病性[98]。而對于BR信號途徑的另一共受體OsSERK1是否參與水稻的免疫反應(yīng),目前存在爭議。Zuo等[99]研究發(fā)現(xiàn)OsSERK1并不參與水稻對M. oryzae和Xoo的防御反應(yīng);而Liao等[100]的結(jié)果顯示OsSERK1正調(diào)控水稻對Xoo的抗性。BSKs(BR-signaling kinase)家族中的OsBSK1-2也參與水稻對稻瘟病的抗病反應(yīng),但并不參與水稻對BR的響應(yīng)[101]。這些結(jié)果表明在水稻中,BR信號途徑中的類受體激酶可能正調(diào)控水稻的抗病反應(yīng)。
也有研究發(fā)現(xiàn)BR在水稻與病原互作中起負調(diào)控作用。外施BL(Brassinolide)可顯著抑制水稻對Pythium graminicola的基礎(chǔ)免疫反應(yīng);而BR合成抑制劑BRZ(Brassinazole)處理則可提高其抗病性,相應(yīng)地,BR合成缺陷突變體的抗病性也明顯減弱;此外,P. graminicola侵染也可激活BR合成途徑和信號,暗示著P. graminicola可能會利用水稻BR系統(tǒng)并作為毒性因子來致?。?02]。RBSDV侵染水稻的過程中,BR合成基因表達下調(diào);同時外施BL在激活BR信號后寄主更感病,而外施BRZ可增強水稻對RBSDV抗病性;此外,與野生型相比,BR信號負調(diào)控基因OsGSK2過表達突變體也更感??;綜上表明BR信號在水稻對RBSDV的免疫反應(yīng)中起負調(diào)控作用[72]。此外,BR在調(diào)控水稻對M. graminicola的免疫反應(yīng)時是依賴于BL濃度的,即外施低濃度BL可增加寄主的感病性,而高濃度BL則提高寄主的抗病性;而BRZ處理和BR合成缺陷均可提高水稻對M. graminicola的抗病性,但僅低濃度BL處理可抑制BR合成缺陷突變體的抗病性[103]。
在擬南芥中 BR和PTI信號之間存在拮抗效應(yīng)[104-106]。這和BR負調(diào)控水稻對P. graminicola、M.graminicola和RBSDV的免疫反應(yīng)一致。至于BR信號途徑中的類受體激酶表現(xiàn)出的正調(diào)控水稻抗病反應(yīng),可能是這些類受體激酶也直接參與了水稻PTI信號激活傳導(dǎo)。在擬南芥中,關(guān)于BAK1協(xié)調(diào)BR和PTI信號的機理目前存在爭論,一種結(jié)果是BRI1和FLS2募集BAK1的過程是獨立的,BR信號抑制PTI信號可能存在其他方式[104],而另一結(jié)果顯示BRI1可能通過和FLS2競爭BAK1以抑制PTI信號[105]。此外,BZR1在BR抑制植物免疫反應(yīng)中也具有重要作用[107];同時BES1可被PTI信號中的MPK6磷酸化,但磷酸化位點和BR信號中不同[108],這些現(xiàn)象顯示BZR1或BES1在權(quán)衡生長和免疫中可能是一個重要的調(diào)節(jié)子。植物在面對外界信號時,生長還是免疫的選擇是需要進行精細調(diào)控的。BR信號也很可能調(diào)控權(quán)衡水稻的生長發(fā)育和免疫防御反應(yīng)。
GAs是一類屬于四環(huán)二萜化合物的植物激素,主要調(diào)控植物的生長發(fā)育過程。在水稻中,GA受體OsGID1結(jié)合具生物活性的GA后可與轉(zhuǎn)錄抑制子DELLA蛋白OsSLR1互作,形成的GA-OsGID1-OsSLR1三聚體可被OsGID2多聚泛素化,隨后OsSLR1被26S蛋白酶系統(tǒng)降解,進而激活GA響應(yīng)的轉(zhuǎn)錄因子[109]。盡管GA最早是在水稻惡苗病的研究過程中發(fā)現(xiàn)的,但是直到近年才逐漸發(fā)現(xiàn)其也參與調(diào)控植物免疫反應(yīng)。GA可誘導(dǎo)水稻對不同病原物產(chǎn)生抗病性和感病性。在水稻和卵菌P. graminicola互作過程中,與野生型相比,GA合成受阻、GA不敏感以及SLR1功能獲得性突變體均表現(xiàn)出增強的感病性,SLR1功能喪失突變體slr1-1的抗病性增強;藥理實驗顯示GA和GA合成抑制劑Uniconazole處理可分別提高和降低水稻的抗病性[103]。Hossain等[110]發(fā)現(xiàn)外源GA的使用可以增加水稻對H.oryzae的抗性。相反地,也有研究報道發(fā)現(xiàn)GA信號可負調(diào)控水稻免疫反應(yīng),外源GA和GA合成抑制劑處理可分別降低和提高水稻對M. oryzae和Xoo的抗病性[111-114]。GA合成基因OsGA20ox3和GA失活蛋白EUI的過表達植株對M. oryzae和Xoo更感病,反之其RNAi干擾植株更抗?。?12-113];GA不敏感突變體和OsSLR1的功能獲得性突變體對M. oryzae或Xoo 的抗病性增強[111,114]。
ABA是一種最先從棉桃中分離出來的物質(zhì),它不僅調(diào)控植物生長發(fā)育的各個階段,還能增強植物的抗逆性。研究發(fā)現(xiàn)ABA處理能顯著抑制水稻對M.oryzae的抗性,ABA不敏感突變體Osabi3表現(xiàn)出對M. oryzae的抗性,表明ABA作為負調(diào)控因子調(diào)控水稻對M. oryzae的抗病性[115-116]。此外,ABA在水稻對Xoo的抗病反應(yīng)中也起負調(diào)控作用[117]。外源噴施ABA,可以抑制C. miyabeanus的生長而增強抵抗能力[118]。
IAA是最早被發(fā)現(xiàn)的植物激素,其不僅參與了水稻的生長發(fā)育過程,在免疫反應(yīng)中也起著重要的作用。有證據(jù)表明,IAA負調(diào)控水稻對病原菌侵染的抗性。用IAA或2,4-D處理水稻后,會刺激Xoo的增殖,導(dǎo)致水稻更感??;同時Xoo的侵染會誘導(dǎo)水稻的IAA積累[120]。在植物中,GH3類蛋白可催化IAA-氨基酸的合成從而抑制生長素的作用。在水稻中,過表達GH3-8、OsGH3.1和GH3-2基因,會降低IAA的含量,導(dǎo)致水稻植株矮小,但增強了水稻對 Xoo、Xanthomonas oryzaepv.oyrzicola(Xoc)和M.oryzae的抗病性[119-121]。此外,過表達OsCYP71Z2也可通過抑制IAA信號以增強對Xoo抗病性[122]。作為平衡植物體內(nèi)生長素的IAA酰胺合成酶GH3s可能作為一個重要的交叉點精細地調(diào)控水稻的生長發(fā)育和防御反應(yīng)。
CKs是最早在玉米種子中發(fā)現(xiàn)的能夠促進細胞分裂的植物激素。盡管目前對CK參與抗病功能研究較少,但也有研究表明CK在植物免疫反應(yīng)中發(fā)揮著重要的作用[123]。研究發(fā)現(xiàn),在接種稻瘟病后的水稻苗中可明顯檢測到CK的積累,同時還發(fā)現(xiàn)病原菌也能產(chǎn)生CK;CK還能協(xié)同SA激活防御反應(yīng),即與水楊酸單獨處理相比,CK和SA共處理更能大幅地提高OsPR1b和PBZ1的表達量,而沉默OsNPR1和OsWRKY45表達后可顯著減弱這種效應(yīng);表明稻瘟病菌能通過提高寄主的CK含量以有利于其侵染,而水稻可能將CK含量的提高作為病原侵染的信號以激活防衛(wèi)反應(yīng)[124]。此外,CK參與調(diào)控番茄、擬南芥和煙草的抗病性[125-129],如在擬南芥中,CK受體AHK3和ARR2調(diào)節(jié)保衛(wèi)細胞的活性氧穩(wěn)態(tài),促進由病原相關(guān)分子模式(PAMP)觸發(fā)的氣孔關(guān)閉,導(dǎo)致擬南芥對丁香假單胞桿菌的抗性增強[127,131]。
在參與水稻抗病反應(yīng)中,植物激素并不是獨立作用于病原物,而是通過激素間的相互拮抗或協(xié)同作用更有效地抵御病原物的侵染。據(jù)報道,過表達OsNPR1增加了植株對水稻對M. oryzae和Xoo的抗性,同時提高了對蟲害的敏感性。OsNPR1過表達植株中OsPR1b的表達被激活,而JA調(diào)控通路的基因OsJAI1的表達被抑制,而且在這個過程中SA和JA的水平并沒有顯著變化,這些結(jié)果暗示OsNPR1調(diào)節(jié)了SA和JA途徑的拮抗作用。ABA可通過抑制SA和ET信號以降低水稻對稻瘟病菌的抗病性,且ABA的負調(diào)控信號位于SA信號途徑WRKY45與NPR1和ET信號EIN2的上游[84]。BR能通過負調(diào)控SA和GA信號而抑制水稻對P. graminicola的基礎(chǔ)免疫反應(yīng)[102],還可通過抑制JA介導(dǎo)的防衛(wèi)反應(yīng)增強對M. graminicola的感病性[104]。在RBSDV侵染水稻過程中,JA信號通路誘導(dǎo)寄主產(chǎn)生的抗病性可通過JA受體COI1抑制BR信號對寄主抗病性的負調(diào)控作用[72]。GA信號中的eui突變體可通過抑制JA信號來負調(diào)控水稻對稻瘟病菌的抗病反應(yīng)[113],SLR1可通過整合和放大依賴于SA和JA的防御反應(yīng)來正調(diào)控對半活體營養(yǎng)型病原菌的防御反應(yīng)[114],即GA可抑制SA和JA介導(dǎo)的防御反應(yīng)。與上述拮抗作用不同的是,JA信號通路和ET信號通路依賴于ERF轉(zhuǎn)錄因子在抵御死體營養(yǎng)型病原菌方面存在協(xié)同作用[131]。線,因此,明確植物激素在水稻內(nèi)的調(diào)控機制對水稻病害的防治具有重要意義?,F(xiàn)代生化和遺傳學方法的結(jié)合,使各種激素的合成,信號轉(zhuǎn)導(dǎo)等機制逐漸清晰化,但現(xiàn)有的研究并沒有解決所有問題。例如:SA合成基因OsICS和OsPAL在內(nèi)源SA的合成和抗病中的作用機制,為什么NPRs與SA結(jié)合的親和力不同?對于JA信號通路而言,其參與調(diào)控防蟲的機理和抗病有何不同?而對于其他植物激素ABA、IAA、CK、BR和GA的研究雖然不多,但是也同樣暴露了研究中存在的不足,雖然現(xiàn)有研究已顯示BR信號途徑參與了調(diào)節(jié)植物免疫反應(yīng),但是關(guān)于其具體調(diào)節(jié)作用和調(diào)控機理仍存在許多不清楚和有爭議之處,尤其是BR信號在水稻中的調(diào)控作用更是需要進一步研究,例如,在水稻免疫反應(yīng)中,BR信號是否也會抑制PTI信號,以及BR信號如何調(diào)控權(quán)衡水稻的生長發(fā)育和免疫反應(yīng)。揭示和明確植物激素如何協(xié)調(diào)自身生長發(fā)育和響應(yīng)外界脅迫及其調(diào)控機理,也將有助于促進農(nóng)業(yè)生產(chǎn),保障糧食安全。
植物激素在植物免疫反應(yīng)中具有重要作用,除了傳統(tǒng)的SA、JA和ET這3種激素,近年來BR和GA等也越來越受到研究者的青睞。幾種植物激素調(diào)控的防御反應(yīng)構(gòu)成了植物抵抗病原物侵染的有效防
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