自然雜志第34卷第4期科技進(jìn)展doi: 103969/j. issn. 0253-9608.2012.04.006乙烯信號(hào)轉(zhuǎn)導(dǎo)通路研究張存立中郭紅衛(wèi)②①博士研究生,②教授,北京大學(xué)生命科學(xué)學(xué)院蛋白質(zhì)與植物基因研究國(guó)家重點(diǎn)實(shí)驗(yàn)室,北京100871關(guān)鍵詞植物激素 乙烯信號(hào)轉(zhuǎn)導(dǎo)作為5大類植物激素之-的乙烯-直是科學(xué)家關(guān)注和研究的焦點(diǎn)。雖然結(jié)構(gòu)簡(jiǎn)單,但是氣態(tài)漱素乙烯在植物的生長(zhǎng)發(fā)育以及脅迫反應(yīng)中具有要的作用。通過(guò)近20年的研究,科學(xué)家已經(jīng)描繪出-條近似線性的乙烯信號(hào)轉(zhuǎn)導(dǎo)通路。在模式植物擬南芥中,這條通路的最上游是由一個(gè)多基因家族編碼的乙烯的5個(gè)受體ETR1, ETR2, ERS1,ERS2和EIN4.與之相結(jié)合并共同定位于內(nèi)質(zhì)網(wǎng)上的是-一個(gè)類似Raf的蛋白激酶CTR1。在沒(méi)有乙烯存在的條件下,受體和CTR1的結(jié)合能夠協(xié)同抑制下游乙烯信號(hào)。在這兩類負(fù)調(diào)控因子的下游是乙烯信號(hào)的正調(diào)控因子EIN2。.如果EIN2基因突變,即使有高濃度乙烯存在,植物黃化苗也將表現(xiàn)出完全的乙烯不敏感表型,顯示出EIN2在乙烯信號(hào)通路中的核心地位。在EIN2的下游是乙烯信號(hào)的轉(zhuǎn)錄因子家族EIN3以及EILs,它們?cè)陧憫?yīng)乙烯信號(hào)之后會(huì)起始乙烯相關(guān)基因的表達(dá)。研究還發(fā)現(xiàn),乙烯的轉(zhuǎn)錄因子受泛素化降解途徑調(diào)控,負(fù)責(zé)識(shí)別及結(jié)合EIN3等轉(zhuǎn)錄因子的F-box蛋自是EBF1和EBF2。EIN5 是一種5'→3'外切核酸酶,它能夠通過(guò)促進(jìn)EBF1和EBF2的mRNA的降解來(lái)拮抗這兩個(gè)F-box蛋白對(duì)EIN3的負(fù)反饋調(diào)控。最近,有研究表明EIN2同樣是一個(gè)半衰期很短并經(jīng)由泛素化降解途徑調(diào)控的蛋自,而執(zhí)行調(diào)控EIN2任務(wù)的是另外兩個(gè)F-box蛋白ETP1和ETP2。雖然人們對(duì)于乙烯信號(hào)轉(zhuǎn)導(dǎo)通路的認(rèn)識(shí)取得了巨大進(jìn)步,但是該信號(hào)通路的精細(xì)調(diào)節(jié)機(jī)制以及乙烯信號(hào)與其他植物激素信號(hào)之間的交叉反應(yīng)還需進(jìn)行更為深入的研究。雖然乙烯是一種結(jié)構(gòu)非常簡(jiǎn)單的氣體植物激素,但乙烯受體相結(jié)合并協(xié)同抑制下游乙烯信號(hào)的是一個(gè)屬是它對(duì)植物發(fā)育以及適應(yīng)性反應(yīng)起著非常重要的作用。于Raf蛋白激酶家族的負(fù)調(diào)節(jié)因子CTR1蛋白[7.8]。遺種子萌發(fā)、開(kāi)花、葉片衰老、果實(shí)成熟、葉片剪切、根瘤、傳上位于CTR1下游的正調(diào)控因子EIN2是一個(gè)定位于細(xì)胞程序性死亡以及對(duì)非生物脅迫和病原體人侵的反內(nèi)質(zhì)網(wǎng)膜.上的大的跨膜蛋白。EIN2 的N端與哺乳動(dòng)物應(yīng)等生理過(guò)程都與乙烯密切相關(guān)[13]。鑒定乙烯反應(yīng)的金屬離子通道蛋白NRAMP家族有一定的相似性;而其特征性實(shí)驗(yàn)是觀察生長(zhǎng)在暗處并經(jīng)乙烯處理之后植物C末端是一個(gè)親水的功能未知的組分。研究發(fā)現(xiàn),EIN2黃化苗的“三重反應(yīng)”。所謂“三重反應(yīng)”是指黃化苗受的C末端與已知蛋白沒(méi)有任何同源性,但是如果在擬南乙烯處理后下胚軸和根的伸長(zhǎng)被抑制、下胚軸變粗以及頂端彎鉤加劇(圖1)。科學(xué)家通過(guò)基于“三重反應(yīng)”進(jìn)行遺傳篩選的方法,在過(guò)去的近20年中找到一系列擬南芥的乙烯突變體(圖2)。這些突變體可以被分為3種類型:①乙烯過(guò)表達(dá)突變體,如eto1, eto2, eto3;②組成型乙烯反應(yīng)突變體，如ctr1;③乙烯不敏感突變體,如etr1, etr2，ein2， ein3, ein4, ein5以及ein61-2.4]。通過(guò)對(duì)這些擬南芥突變體的深入研究,科學(xué)家逐漸描繪出一條近似線性的乙烯信號(hào)轉(zhuǎn)導(dǎo)通路(圖3)。首先,在上游對(duì)乙烯分子的感知是通過(guò)一個(gè)與內(nèi)質(zhì)網(wǎng)膜相結(jié)合的受體家族來(lái)完成的,其中包括ETR1, ETR2, ERS1,中國(guó)煤化工ERS2 ,EIN4。這些乙烯受體在序列上具有相似性,并且在結(jié)構(gòu).上都與細(xì)菌雙組分組蛋白激酶相類似[3.5.6]。與CHCNMHG長(zhǎng)仕CT(入)的“三重反應(yīng)"表型，219●ProgressChinese Journal of Nature Vol, 34 No. 4黃花苗成株作為一個(gè)正調(diào)控因子,其抑制被解除后即可通過(guò)正調(diào)乙烯信號(hào)途徑的主要轉(zhuǎn)錄因子EIN3和EIL1而將信號(hào)通過(guò)轉(zhuǎn)錄級(jí)聯(lián)方式傳遞下去,使得下游乙烯應(yīng)答基因的轉(zhuǎn)錄被活化而產(chǎn)生乙烯反應(yīng)10-11]。近年來(lái),一些新的科研成果進(jìn)- -步豐富和擴(kuò)展了乙烯的線性信號(hào)轉(zhuǎn)導(dǎo)通路。研究表明,銅離子作為一個(gè)輔助因子促進(jìn)乙烯與受體的結(jié)合,而銅離子的轉(zhuǎn)運(yùn)和濃度梯度的維持對(duì)于乙烯與受體的結(jié)合是一個(gè)必要的過(guò)程。-種具有銅離子轉(zhuǎn)運(yùn)功能的P-type ATPase RAN1在乙烯受體的生物發(fā)生以及銅離子的穩(wěn)態(tài)平衡過(guò)程中起到重要的調(diào)節(jié)作用[12]。RTE1是另-類對(duì)受體功能起調(diào)節(jié)作用的乙烯信號(hào)的負(fù)調(diào)控蛋白,它與乙烯受體共定位于內(nèi)質(zhì)網(wǎng)膜上并在遺傳上位于ETR1的上游,主要通過(guò)調(diào)節(jié)ETR1的活性來(lái)調(diào)節(jié)乙烯反應(yīng)13.14]。研究表明,EIN3蛋白可被兩個(gè)F-box蛋白EBF1和EBF2識(shí)別結(jié)合并進(jìn)人泛素化降解過(guò)程[5-17]。有趣的是,研究表明EIN2同樣是-一個(gè)半衰期很短的會(huì)被泛素化降解的蛋白,識(shí)別和降解EIN2蛋白圈2野生型.乙烯不敏感突變體及組成型乙烯的F-box蛋白是ETP1和ETP2[18]。5'→3'外切核酸酶反應(yīng)突變體黃化苗和成株表型EIN5/XRN4蛋白能夠通過(guò)降解EBF1和EBF2的mR-芥中單獨(dú)轉(zhuǎn)基因表達(dá)該區(qū)段卻足以組成型地激活乙烯NA來(lái)拮抗EBF1 和EBF2對(duì)EIN3的負(fù)反饋調(diào)和脅迫反應(yīng)[9]。表型、遺傳以及生化的分析結(jié)果都顯示控[9.20。近期,關(guān)于EIN3蛋白磷酸化修飾調(diào)節(jié)的研究EIN2蛋白位于乙烯信號(hào)通路的一個(gè)中心位置。EIN2揭示出更為復(fù)雜的激素調(diào)控網(wǎng)絡(luò)的存在[21-22]。Golg/EREthylene民MPS/ERS2EIN4Cytoplasm|CTRIRNudeus, Ethylene ResponseEFLEBFZ,HUSL,PORA中國(guó)煤化工圖3乙烯信號(hào)轉(zhuǎn)導(dǎo)通路示意TYHCNM HG●220●自然雜志第34卷第4期科技進(jìn)展的參與,而在此過(guò)程中負(fù)責(zé)銅離了轉(zhuǎn)運(yùn)和濃度梯度維持1乙烯受體及其對(duì)乙烯信號(hào)的感知的蛋白是一個(gè)具有P-type ATPase 活性的RAN1蛋白[12。RTE1是另一類進(jìn)化上非常保守的膜結(jié)合蛋白，植物細(xì)胞通過(guò)定位于內(nèi)質(zhì)網(wǎng)上的受體感知乙烯信其轉(zhuǎn)錄活性受乙烯調(diào)控,并且RTE1通過(guò)與乙烯受體相號(hào)。在擬南芥中共有由一個(gè)多基因家族編碼的5個(gè)乙互作用而負(fù)調(diào)控乙烯反應(yīng),暗示乙烯信號(hào)的感知可能存烯受體,分別是ETR1, ETR2, ERS1, ERS2和EIN4.在更為精細(xì)的調(diào)節(jié)過(guò)程[13.35]。它們?cè)诮Y(jié)構(gòu)上類似于細(xì)菌和真菌中存在的雙組分組蛋白激酶5-6.23]。通過(guò)比較其結(jié)構(gòu)特征,發(fā)現(xiàn)乙烯受體存在至少3類保守的結(jié)構(gòu)域:N端是一一個(gè)在銅離子協(xié)助下2 CTR1激酶及其可能介導(dǎo)的MAPK途徑與乙烯結(jié)合的跨膜結(jié)構(gòu)域;中間是一個(gè)負(fù)責(zé)不同受體間與乙烯受體結(jié)合并協(xié)同抑制下游乙烯反應(yīng)的是另相互作用的GAF結(jié)構(gòu)域;C端是一個(gè)能與下游組分一個(gè)負(fù)調(diào)節(jié)因子CTR1蛋白。ctr1突變體會(huì)表現(xiàn)出組CTR1相互作用的激酶結(jié)構(gòu)域。乙烯5個(gè)受體可根據(jù)其成型的乙烯反應(yīng)表型[7]。序列分析顯示CTR1蛋白是結(jié)構(gòu)相似性被分為兩大類，一類受體包括ETR1和類似于哺乳動(dòng)物Raf家族的絲氨酸/蘇氨酸蛋白激酶。ERS1 ,另一類受體包括ETR2, ERS2和EIN4[6.24J。研CTR1通過(guò)其氨基端與內(nèi)質(zhì)網(wǎng)上的乙烯受體的羧基端相究表明,乙烯受體的N端涉及受體的膜定位、乙烯結(jié)合結(jié)合而被間接錨定在內(nèi)質(zhì)網(wǎng)膜上,從而形成受體.以及受體的二聚化等基本功能,因此5個(gè)乙烯受體在N端具有較高的相似性(25-26]。乙烯受體的C端則是類似CTR1復(fù)合體,而且CTR1對(duì)下游乙烯信號(hào)的負(fù)調(diào)控功于組蛋白激酶的結(jié)構(gòu)域。但是,體外激酶活性實(shí)驗(yàn)表明能是依賴于這一-蛋白相互作用的[8,36-37]。研究表明，僅有ETR1, ERS1具有組蛋白激酶活性;其他受體CTR1的羧基端具有絲氨酸/蘇氨酸蛋白激酶活性,而激ETR2,ERS2和EIN4則由于缺少組蛋白激酶活性所必酶失活的ctr1突變體將會(huì)表現(xiàn)出組成型乙烯反應(yīng)表需的氨基酸殘基而可能作為絲氨酸/蘇氨酸蛋白激酶來(lái)型[37]。起作用[27-28]。CTR1的功能依賴于其與乙烯受體的結(jié)合。研究發(fā)由于乙烯結(jié)合能力發(fā)生突變而產(chǎn)生的受體功能獲現(xiàn),由于氨基端發(fā)生錯(cuò)義突變而破壞了與受體結(jié)合能力得型突變體將會(huì)導(dǎo)致組成型乙烯不敏感表型的出現(xiàn),表的CTR1即便其羧基端激酶活性不受影響,仍然不能再明乙烯受體作為乙烯信號(hào)的負(fù)調(diào)控因子而存對(duì)下游乙烯信號(hào)產(chǎn)生抑制作用[37]?；贑TR1在序列在(5.23.29-30]。同時(shí),乙烯的5個(gè)受體存在功能上的冗上與Raf蛋白激酶的相似性,人們很容易聯(lián)想到CTR1余,因?yàn)閱蝹€(gè)受體的功能缺失型突變體表型與野生型類在乙烯信號(hào)通路中是否作為一種MAPKKK通過(guò)介導(dǎo)似,但多重功能缺失突變體則具有組成型的乙烯反應(yīng)表-條MAPK級(jí)聯(lián)反應(yīng)而激活下游乙烯信號(hào)。雖然生化型[31]。進(jìn)一步研究發(fā)現(xiàn),轉(zhuǎn)基因表達(dá)類型I受體ETR1證據(jù)顯示乙烯反應(yīng)能夠影響植物細(xì)胞內(nèi)的磷酸化水平，或ERS1能夠回復(fù)功能缺失型雙突變體etr1/ers1的組但是之前的研究沒(méi)有直接證據(jù)證明乙烯信號(hào)通路存在成型乙烯反應(yīng)表型;轉(zhuǎn)基因表達(dá)類型II受體ETR2,一條由CTR1介導(dǎo)的激活下游乙烯信號(hào)通路的MAPKERS2或EIN4卻不能回復(fù)etr1/ers1 雙突變體的組成途徑[38-40]。有趣的是，多種證據(jù)卻表明細(xì)胞內(nèi)存在-型乙烯反應(yīng)表型(32]?？茖W(xué)家猜測(cè)是否因?yàn)轭愋虸受體條MKK4/5/9-MPK3/6途徑通過(guò)修飾乙烯生物合成限獨(dú)特的組氨酸激酶活性導(dǎo)致了其對(duì)功能缺失型雙突變速酶ACS2/6的穩(wěn)定性而在乙烯生物合成水平而非乙體表型的回復(fù)作用。但是,轉(zhuǎn)基因表達(dá)組氨酸激酶失活烯信號(hào)轉(zhuǎn)導(dǎo)水平對(duì)乙烯反應(yīng)進(jìn)行調(diào)節(jié)[41441。近期,有的ETR1仍然可以回復(fù)功能缺失型雙突變體etr1/ers1研究小組認(rèn)為在擬南芥原生質(zhì)體中CTR1可以繞過(guò)下的表型,說(shuō)明組氨酸激酶活性并不是類型I受體抑制乙烯信號(hào)所必需的,而可能只是參與了乙烯信號(hào)的某些調(diào)游正調(diào)控因子EIN2蛋白而直接通過(guò)MKK9-MPK3/6節(jié)過(guò)程256.33.還有研究表明,即便受體缺失整個(gè)羧基控制乙烯信號(hào)的轉(zhuǎn)錄因子EIN3蛋白的磷酸化而使其失端包括組氨酸激酶區(qū)和信號(hào)接受區(qū),功能獲得型的受體活,從而抑制下游乙烯信號(hào)[21]。但是,另一組科學(xué)家在ETR1仍然具有抑制下游乙烯信號(hào)的功能，說(shuō)明受體用對(duì)應(yīng)的MKK9基因突變體以及轉(zhuǎn)基因過(guò)表達(dá)植株進(jìn)ETR1的C端對(duì)于其抑制功能并非必需[2]?？茖W(xué)家因行實(shí)驗(yàn)時(shí)卻表明，在擬南芥體內(nèi)MKK9并非繞過(guò)EIN2此推測(cè)乙烯受體之間可以通過(guò)相互協(xié)同作用而維持受蛋白而直中國(guó)煤化工作用于乙烯生物合體的抑制功能[25.27.34]。乙烯與受體的結(jié)合需要銅離子成途徑而YHCNMHG221●ProgressChinese Journal of Nature Vol, 34 No. 4同源性:最高,功能上也最為相似[10.22]。研究發(fā)現(xiàn)，EIN33 EIN2跨膜蛋白及其謎一.樣的功能與EIL1雙基因突變形成的突變體ein3/eil1 與ein2-樣在黃化苗時(shí)期和成年植株中能夠表現(xiàn)出完全的乙烯EIN2蛋白位于CTR1的下游,是乙烯信號(hào)通路中不敏感表型，說(shuō)明這兩個(gè)轉(zhuǎn)錄因子負(fù)責(zé)大部分的乙烯信的第一個(gè)正調(diào)控組分?？茖W(xué)家在20多年前篩選乙烯突號(hào)傳遞1[10.30]。同時(shí),單獨(dú)轉(zhuǎn)基因過(guò)量表達(dá)EIN3或者變體時(shí)篩到了它[45]。EIN2基因發(fā)生功能缺失型突變EILI,乙烯信號(hào)途徑都能被組成型地活化;但是,單基因可以產(chǎn)生完全的乙烯不敏感表型,暗示EIN2 在乙烯信功能缺失突變體ein3-1 或eil1-1都只表現(xiàn)出部分乙烯號(hào)轉(zhuǎn)導(dǎo)通路中的核心地位[9]。序列分析表明，EIN2基不敏感的表型,說(shuō)明EIN3及其家族成員不僅正調(diào)乙烯因編碼一個(gè)12跨膜的大的膜結(jié)合蛋白,其N端定位于反應(yīng)而且在功能上存在冗余[10]。除了EIL1,擬南芥中內(nèi)質(zhì)網(wǎng)膜上,C端則游離在胞質(zhì)中[9.46]。進(jìn)一步研究發(fā)還有另外4個(gè)EIN3類似蛋白EIL2-EIL5,可能涉及早現(xiàn),EIN2蛋白的N端類似于具有轉(zhuǎn)運(yùn)二價(jià)陽(yáng)離子功能期乙烯反應(yīng)的調(diào)節(jié)過(guò)程[51]。的NRAMP離子通道家族蛋白;與N端不同是, EIN2轉(zhuǎn)錄因子EIN3和EIL1在細(xì)胞核內(nèi)通過(guò)啟動(dòng)轉(zhuǎn)錄.的C端為一親水區(qū),而且序列分析表明EIN2的C端與級(jí)聯(lián)反應(yīng)而激活乙烯應(yīng)答基因的表1.1.52.555研究其他已知蛋白相比沒(méi)有明顯的序列相似性，暗示出發(fā)現(xiàn),EIN3能夠通過(guò)二聚化的方式特異性地與一個(gè)被EIN2蛋白的C端可能具有非常獨(dú)特的功能[9]。稱為EIN3結(jié)合位點(diǎn)(EIN3bindingsite,EBS)的短的回雖然EIN2蛋白的N端類似于NRAMP離子通道,文結(jié)構(gòu)啟動(dòng)子區(qū)域相結(jié)合并啟動(dòng)ERF1,EDF1-4等初級(jí)但是沒(méi)有實(shí)驗(yàn)證據(jù)表明EIN2的N端確實(shí)具有離子轉(zhuǎn)轉(zhuǎn)錄因子的表達(dá);而ERF1可以進(jìn)一步與啟動(dòng)子區(qū)含運(yùn)能力,EIN2的N端在乙烯信號(hào)轉(zhuǎn)導(dǎo)通路中的功能還GCC-box的次級(jí)乙烯應(yīng)答基因結(jié)合并起始其轉(zhuǎn)錄1[1]。有待研究[9?？茖W(xué)家在研究EIN2的功能時(shí)還發(fā)現(xiàn),如.有趣的是,研究發(fā)現(xiàn)對(duì)轉(zhuǎn)錄因子EIN3本身的調(diào)節(jié)發(fā)生果轉(zhuǎn)基因過(guò)量表達(dá)EIN2蛋白的全長(zhǎng)或者其N端,擬南在蛋白水平而非轉(zhuǎn)錄水平上[10]。在乙烯信號(hào)通路中,由芥暗中或者光下的乙烯反應(yīng)表型都不能被恢復(fù);但是，26S蛋白酶體所介導(dǎo)的泛素化降解途徑調(diào)節(jié)了EIN3蛋轉(zhuǎn)基因單獨(dú)過(guò)量表達(dá)EIN2蛋白的C端卻能夠恢復(fù)擬南白的穩(wěn)定性,而負(fù)責(zé)識(shí)別和結(jié)合轉(zhuǎn)錄因子EIN3的有兩個(gè)芥光下生長(zhǎng)的幼苗以及成年植株的乙烯反應(yīng)表型[9]。Fbox蛋白EBF1和EBF2[16-17]。EBF1 和EBF2通過(guò)介因此,EIN2蛋白可能是一個(gè)雙功能信號(hào)組分:N端負(fù)責(zé)導(dǎo)EIN3等轉(zhuǎn)錄因子降解過(guò)程而對(duì)乙烯信號(hào)進(jìn)行負(fù)接受.上游乙烯信號(hào),而且參與乙烯的暗形態(tài)反應(yīng);C端調(diào)[15.17]。 另外,EIN3等乙烯轉(zhuǎn)錄因子還受到負(fù)反饋調(diào)節(jié)則負(fù)責(zé)激活下游乙烯信號(hào)[9]。雖然研究發(fā)現(xiàn)擬南芥中機(jī)制的調(diào)控,因?yàn)橐蚁┨幚砟軌蛲瑫r(shí)上調(diào)EBF2的轉(zhuǎn)錄量EIN2蛋白與乙烯受體.COP9光信號(hào)復(fù)合體組分EER5從而使乙烯反應(yīng)不至于過(guò)強(qiáng)[15.53]。近期研究還發(fā)現(xiàn)- -等蛋白具有一-定相互作用,對(duì)EIN2功能的研究提供了個(gè)具有5'→3'外切核酸酶活性的蛋白EIN5/XRN4可以-定線索,但是EIN2所介導(dǎo)的乙烯信號(hào)傳遞機(jī)制仍是通過(guò)促進(jìn)EBF1/EBF2的mRNA的降解來(lái)拮抗EBF對(duì)一個(gè)謎團(tuán)[4-48]。近期,科學(xué)家發(fā)現(xiàn)EIN2蛋白也是一種EIN3的負(fù)反饋調(diào)控,這一發(fā)現(xiàn)大大擴(kuò)展了人們對(duì)于乙烯短周期蛋白,可被兩個(gè)F-box 蛋白ETP1和ETP2識(shí)別信號(hào)調(diào)控水平多樣性和復(fù)雜性的認(rèn)識(shí)[1].并經(jīng)由蛋白酶體依賴的泛素化降解途徑而降解[18]。此外,在篩選其他激索如生長(zhǎng)素、細(xì)胞分裂素和脫落酸等5乙烯信號(hào)與其他信號(hào)通路的交叉反應(yīng)信號(hào)途徑的突變體時(shí)也能夠篩到對(duì)應(yīng)于EIN2基因的突變體,暗示EIN2可能涉及多個(gè)激素信號(hào)之間的交叉反盡管人們對(duì)于乙烯信號(hào)轉(zhuǎn)導(dǎo)通路的認(rèn)識(shí)正在逐步應(yīng)49-50]。由此可見(jiàn),EIN2蛋白不僅對(duì)于乙烯信號(hào)至關(guān)清晰,但是對(duì)于植物多樣化乙烯效應(yīng)的下游分子網(wǎng)絡(luò)還重要,而且還參與不同激素信號(hào)途徑之間的交叉反應(yīng)。知之甚少,而乙烯與其他信號(hào)途徑的交叉反應(yīng)為多樣化的乙烯反應(yīng)提供了最為重要的解釋[54]。研究表明,乙4 EIN3/EILs在轉(zhuǎn)錄水平對(duì)乙烯信號(hào)烯信號(hào)與生長(zhǎng)素(auxin)、細(xì)胞分裂素(cytokinin,CK)、赤霉素( gibberellin ,GA)、脫落酸(abscisic acid, ABA).的調(diào)控油菜素內(nèi)脂(brassinosteroid, BR)、 茉莉酸( jasmonic乙烯信號(hào)經(jīng)過(guò)傳遞最終被匯聚到位于EIN2蛋白下acid, JA)、水楊酸(salicylic acid, SA) 等植物激素及植游的轉(zhuǎn)錄因子家族EIN3以及5個(gè)EILs(EIN3-ike pro-物生長(zhǎng)因中國(guó)煤化工及營(yíng)養(yǎng)因子存在著teins)等正調(diào)控因子。在5個(gè)EILs中,EIL1與EIN3的廣 泛的聯(lián)YHCNMHG協(xié)同，在植物的生自然雜志第34卷第4期科技進(jìn)展長(zhǎng)發(fā)育以及植物應(yīng)對(duì)生物、非生物脅迫等復(fù)雜過(guò)程中起1)[66]。HSS1 基因編碼-一個(gè)生長(zhǎng)素應(yīng)答轉(zhuǎn)錄因子ARF2到非常重要的作用。(Auxin Response Factor 2),而ARF2對(duì)于在HLS1下游調(diào)節(jié)差異化細(xì)胞伸長(zhǎng)以及頂端彎鉤形成是必需5.1乙烯與生長(zhǎng)素的[66。乙烯處理能夠下調(diào)ARF2的蛋白水平,而且這人們?cè)缫阎酪蚁┖蜕L(zhǎng)素在根的伸長(zhǎng)、下胚軸的-過(guò)程是HLS1依賴的。綜上所述,生長(zhǎng)素應(yīng)答轉(zhuǎn)錄因差異化生長(zhǎng)以及根毛形成等多種生物學(xué)過(guò)程中存在廣子ARF2通過(guò)抑制差異化的生長(zhǎng)素效應(yīng)而抑制頂端彎泛的交叉反應(yīng)[55]。研究發(fā)現(xiàn),許多在根上特異的乙烯鉤的形成;而乙烯通過(guò)激活其上游的HLS1蛋白負(fù)調(diào)不敏感突變體,其生長(zhǎng)素的合成或者轉(zhuǎn)運(yùn)也存在缺陷，ARF2的功能,從而促進(jìn)頂端彎鉤的形成。暗示乙烯可能通過(guò)調(diào)節(jié)生長(zhǎng)素信號(hào)來(lái)抑制植物根的伸長(zhǎng)[56-57]。兩個(gè)在根上特異的乙烯不敏感突變體wei25.2乙烯與細(xì)胞分裂素和wei7 的發(fā)現(xiàn)把乙烯信號(hào)和生長(zhǎng)素信號(hào)聯(lián)系起除了生長(zhǎng)素,其他激素也可以誘導(dǎo)乙烯生物合成量來(lái)[58-59]。WEI2 和WEI7 分別編碼色氨酸生物合成的的提高,例如細(xì)胞分裂素[67.68]。生長(zhǎng)素處理可以導(dǎo)致關(guān)鍵酶鄰氨基苯甲酸合成酶的a和β亞基,而色氨酸是幾個(gè)ACS蛋白轉(zhuǎn)錄量的增加,而細(xì)胞分裂素可以增加多個(gè)生長(zhǎng)素生物合成途徑的共同前體[59]。乙烯通過(guò)激ACS5蛋白的穩(wěn)定性67.69-70]。另一組科學(xué)家的研究顯活WEI2和WEI7基因的表達(dá)促進(jìn)了根中生長(zhǎng)素的合示細(xì)胞分裂素可以增加一些ACS基因的穩(wěn)定性[71]。此成和積累,從而抑制了植物根的伸長(zhǎng)。更為直接的證據(jù)外,細(xì)胞分裂素對(duì)乙烯的誘導(dǎo)依賴于典型的細(xì)胞分裂素來(lái)自于另一個(gè)根特異的乙烯不敏感突變體wei8 的發(fā)雙組分應(yīng)答通路的存在，包括組氨酸激酶、組氨酸磷酸現(xiàn)[60]。WEI8基因負(fù)責(zé)編碼生長(zhǎng)素生物合成途徑中的色轉(zhuǎn)移蛋白以及應(yīng)答調(diào)節(jié)因子等的存在。這些結(jié)果說(shuō)明，氨酸氨基轉(zhuǎn)移酶TAA1。研究發(fā)現(xiàn),乙烯處理能夠通過(guò)特乙烯生物合 成途徑的限速酶ACS可以被多種激素包括異地在根部分生區(qū)促進(jìn)TAA1及其同源基因TAR2的表乙烯、生長(zhǎng)素、細(xì)胞分裂素等通過(guò)不同的信號(hào)通路介人達(dá)促進(jìn)生長(zhǎng)素lAA(indole-3-acetic acid) 的生物合成,從進(jìn)行調(diào)節(jié),這可能由植物自身組織的特異性及其對(duì)不同而抑制了根的伸長(zhǎng)。另外,乙烯三重反應(yīng)的短根表型不環(huán)境條件的響應(yīng)來(lái)調(diào)節(jié)乙烯的生物合成量。僅與乙烯調(diào)控的生長(zhǎng)素在局部的生物合成相關(guān),還與乙烯調(diào)控的生長(zhǎng)素從分生區(qū)到伸長(zhǎng)區(qū)的分布相關(guān)[61-63]。5.3乙烯與赤霉素如前所述,乙烯可以通過(guò)促進(jìn)生長(zhǎng)素的合成來(lái)抑制植物赤霉素也是植物生長(zhǎng)和發(fā)育過(guò)程中所必需的一種根的伸長(zhǎng)。反過(guò)來(lái),生長(zhǎng)素也可以通過(guò)誘導(dǎo)乙烯合成基植物激素。有一個(gè)研究組報(bào)道,乙烯和赤霉素的交叉反因ACS4的表達(dá)而促進(jìn)乙烯的生物合成[64]。研究發(fā)現(xiàn)，應(yīng)會(huì)影響歐洲山毛櫸(FagussylvaticaL.)種子由休眠到在黃化苗中ACS4基因可以特異地被lAA誘導(dǎo);同時(shí),在萌發(fā)的轉(zhuǎn)換[72]。他們發(fā)現(xiàn)用GA3或者乙烯利處理山擬南芥生長(zhǎng)素抗性突變體axr1-12， axr2-1以及aux1-7毛櫸的種子之后其乙烯生物合成酶 FsACO1基因的表中ACS4基因的表達(dá)存在缺陷[64]。達(dá)大幅上調(diào),但是乙烯利的調(diào)節(jié)效應(yīng)可以被GA的生物在頂端彎鉤的發(fā)育上,生長(zhǎng)素和乙烯同樣存在交叉合成抑制劑多效唑逆轉(zhuǎn),說(shuō)明GA正調(diào)控FsACO1基因反應(yīng)。在篩選擬南芥乙烯信號(hào)遺傳突變體時(shí),科學(xué)家發(fā)的表達(dá)[2]。GA信號(hào)通路的一個(gè)關(guān)鍵事件即能夠與現(xiàn)一個(gè)特異的僅在頂端彎鉤對(duì)乙烯不敏感的突變體GA受體GID1相互作用的負(fù)調(diào)控因子DELLA蛋白在.hIs1[45]。 過(guò)表達(dá)HLS1基因能夠產(chǎn)生組成型的下胚軸響應(yīng)GA之后的降解。DELLA蛋白在維持植物體內(nèi)彎鉤表型。乙烯處理能夠激活HLS1基因的轉(zhuǎn)錄，而在GA的動(dòng)態(tài)平衡以及在調(diào)節(jié)GA與其他植物激素信號(hào)的ein2突變體中HLS1 基因表達(dá)下調(diào)[65]。研究表明，交 叉反應(yīng)過(guò)程中也發(fā)揮著重要作用[73]。在GA存在的hls1突變體對(duì)應(yīng)的基因HLS1編碼的蛋白屬于N-乙酰情況下,DELLA蛋白被降解,從而下游GA反應(yīng)的抑制轉(zhuǎn)移酶家族成員[65]。此外,HLS1蛋白的缺失可以導(dǎo)致被解除。有科學(xué)家觀察到乙烯處理可以延遲GA介導(dǎo)子葉和下胚軸彎鉤區(qū)域生長(zhǎng)素調(diào)節(jié)基因出現(xiàn)異常的表的依賴于CTR1的GFP-RGA從根細(xì)胞核內(nèi)的消失，說(shuō)達(dá)663]。以上結(jié)果表明,HLS1可能通過(guò)抑制子葉和下胚明乙烯處理可以穩(wěn)定DELLA蛋白[74]。相似地,還有軸彎鉤區(qū)域生長(zhǎng)素誘導(dǎo)的細(xì)胞伸長(zhǎng)而介導(dǎo)頂端彎鉤的報(bào)道稱乙烯可以通過(guò)調(diào)節(jié)DELLA依賴的花分生組織形成。為進(jìn)一步研究HLS1基因介導(dǎo)的頂端彎鉤形成特異性基因來(lái)控制龍期轉(zhuǎn)掘[75].7烯信號(hào)的激活可以的分子機(jī)制,科學(xué)家在hls1突變體的基礎(chǔ)上篩選到一個(gè)減少具有中國(guó)煤化工可以促進(jìn)DELLA可以抑制該突變表型的突變體hss1( HLS1 suppressor蛋白的積MHCNMHG而可以延緩植物生223.ProgressChinese Journal of Nature Vol. 34 No. 4命周期,并且可以通過(guò)抑制花分生組織特異性基因且在頂端彎鉤建立油菜素內(nèi)脂的濃度梯度來(lái)促進(jìn)彎鉤LEAFY和SOC1的表達(dá)延遲開(kāi)花[75]。最近有研究表的形成80-81]。在控制下胚軸伸長(zhǎng)方面,最近的研究發(fā)明,GA也能夠通過(guò)誘導(dǎo)HLS1的表達(dá)而使黃化苗頂端現(xiàn)油菜素內(nèi)脂可能通過(guò)其信號(hào)途徑中的一個(gè)受體樣蛋彎鉤加劇[76]。沒(méi)有GA時(shí),DELLA蛋白能夠與EIN3白激酶FERONIA來(lái)調(diào)節(jié)乙烯反應(yīng)的強(qiáng)度,以此調(diào)節(jié)擬的DNA結(jié)合結(jié)構(gòu)域互作從而抑制了EIN3 對(duì)HLS1基南芥下胚軸的長(zhǎng)度[82]。另外,油菜素內(nèi)脂處理可以使因的轉(zhuǎn)錄;施加GA之后,DELLA對(duì)EIN3的轉(zhuǎn)錄抑制乙烯生物合成增加[67]。近期研究發(fā)現(xiàn)，和細(xì)胞分裂素效應(yīng)被解除,HLS1基因的表達(dá)被啟動(dòng)，從而促進(jìn)了頂端類似,油菜素內(nèi)脂能夠通過(guò)促進(jìn)ACS基因轉(zhuǎn)錄以及穩(wěn)彎鉤的形成[76]。定ACS5蛋白來(lái)增加乙烯的生物合成[71]。5.4乙烯與脫落酸5.6乙烯與茉莉酸科學(xué)家在篩選ABA突變體時(shí)發(fā)現(xiàn)-個(gè)能夠使種子乙烯和茉莉酸之間同樣存在著復(fù)雜的交叉反應(yīng)，既在萌發(fā)過(guò)程中對(duì)ABA敏感性增強(qiáng)的突變體era3是由相互拮抗,又相互協(xié)同。一方面,乙烯可以強(qiáng)烈抑制茉于乙烯信號(hào)核心組分EIN2基因突變所致,揭示出ABA莉酸介導(dǎo)的損傷應(yīng)答基因的轉(zhuǎn)錄,茉莉酸反過(guò)來(lái)也可以信號(hào)在此過(guò)程中與乙烯信號(hào)相互作用并且受到乙烯信抑制乙烯介導(dǎo)的頂端彎鉤形成,說(shuō)明兩種激素之間在一號(hào)的負(fù)調(diào)77]。實(shí)際上,當(dāng)時(shí)有兩個(gè)獨(dú)立的課題組分別定條件下可能相互拮抗83-84]。另一方面,在抵抗真菌篩選可能影響ABA信號(hào)通路的突變并且都鑒定到了乙感染時(shí)二者又可以協(xié)同作用,植物受到真菌感染即可快烯信號(hào)的突變體77.7]。此外,實(shí)驗(yàn)顯示ctr1 和ein2突速產(chǎn)生乙烯和茉莉酸并使下游防御基因的表達(dá)升高，例變體分別對(duì)abi1突變體起增強(qiáng)和抑制作用;其他乙烯如ERF1, ORA59 以及PDF1.2 等防御基因85-87?？撇幻舾型蛔凅w也表現(xiàn)出增強(qiáng)的ABA反應(yīng),進(jìn)-步說(shuō)明學(xué)家發(fā)現(xiàn),如果單獨(dú)用乙烯或者茉莉酸處理植物即可分在擬南芥種子中乙烯作為ABA信號(hào)的一個(gè)負(fù)調(diào)節(jié)因子別誘導(dǎo)防御基因的較高水平的表達(dá);有趣的是,如果兩存在778。與種子中的效應(yīng)相反，同樣這些在種子中種激素同時(shí)施加則會(huì)使下游防御基因的表達(dá)量達(dá)到最表現(xiàn)出增強(qiáng)的ABA反應(yīng)的乙烯不敏感突變體在根上卻高值,說(shuō)明在誘導(dǎo)防御基因表達(dá)上兩者具有協(xié)同效表現(xiàn)出對(duì)ABA反應(yīng)的降低77-7]。更為復(fù)雜的是,研究應(yīng)85.88]。此外,無(wú)論是用乙烯、菜莉酸單獨(dú)處理或者兩發(fā)現(xiàn)雖然外源ABA沒(méi)有影響到乙烯的生物合成,但是者同時(shí)處理乙烯不敏感突變體ein2以及茉莉酸不敏感乙烯合成增加突變體可以產(chǎn)生一個(gè)與乙烯不敏感突變突變體coi1都無(wú)法再誘導(dǎo)下游防御基因的表達(dá),暗示植體相似的在根上對(duì)ABA不敏感的表型。很難想像乙烯物防御反應(yīng)的激活依賴于乙烯和茉莉酸兩種信號(hào)通路反應(yīng)降低和乙烯合成增加都能夠在根對(duì)ABA的反應(yīng)上的同時(shí)存在88-89。最近,科學(xué)家發(fā)現(xiàn)茉莉酸信號(hào)通路產(chǎn)生相同的效應(yīng),但是這也進(jìn)-.步暗示在擬南芥中的負(fù)調(diào)控因子JAZ蛋白能夠通過(guò)募集一個(gè)RPD3類型ETR1應(yīng)答途徑可能調(diào)控了不依賴于乙烯的信號(hào)。除了的組蛋白去乙?；窰DA6調(diào)節(jié)組蛋白的乙酰化進(jìn)而種子和根,有科學(xué)家在氣孔開(kāi)閉研究過(guò)程中同樣發(fā)現(xiàn)乙抑制乙烯信號(hào)轉(zhuǎn)錄因子EIN3/EIL1依賴的基因轉(zhuǎn)錄，烯和脫落酸存在相互作用[79]。他們用乙烯過(guò)表達(dá)突變從而抑制了茉莉酸信號(hào)通路[0]。研究發(fā)現(xiàn)，與施加乙體eto1-1以及乙烯不敏感突變體etr1-1, ein3-1 研究烯可以使EIN3/EIL1蛋白穩(wěn)定一樣,施加茉莉酸也可發(fā)現(xiàn),乙烯能夠抑制ABA誘導(dǎo)的氣孔關(guān)閉[79]。這一結(jié)以通過(guò)促進(jìn)JAZ蛋白的降解而穩(wěn)定轉(zhuǎn)錄因子EIN3/果進(jìn)一步說(shuō)明乙烯和脫落酸存在著廣泛而復(fù)雜的交叉EIL190]。另-方面,如果乙烯信號(hào)被阻斷,轉(zhuǎn)錄因子反應(yīng),而且其相互作用在不同組織及發(fā)育階段具有不同EIN3/EIL1將會(huì)被迅速降解而導(dǎo)致植物對(duì)乙烯和茉莉的效應(yīng)。酸均不敏感;而當(dāng)茉莉酸信號(hào)被阻斷時(shí),將導(dǎo)致JAZ蛋白的大量積累進(jìn)而強(qiáng)烈抑制轉(zhuǎn)錄因子EIN3/EIL1的功5.5乙烯與油菜素內(nèi)脂能,同樣會(huì)致使植物對(duì)乙烯和茉莉酸不敏感表型的出油菜素內(nèi)脂近年也得到了廣泛的研究，被稱為第六現(xiàn)[90]。以上結(jié)果表明,乙烯信號(hào)轉(zhuǎn)錄因子EIN3/EIL1大植物激素。與其他五大類植物激素相比,油菜素內(nèi)脂可能是乙烯和茉莉酸信號(hào)通路的交叉結(jié)點(diǎn)。具有獨(dú)特的生理活性,而且含量極低即可發(fā)揮生理效5.7乙烯與水楊酸應(yīng)。近期的研究發(fā)現(xiàn),油菜素內(nèi)脂與乙烯信號(hào)在下胚軸中國(guó)煤化工伸長(zhǎng)以及頂端彎鉤形成等方面存在著相互作用及功能植物MH素,即水楊酸、茉莉冗余[80]。乙烯能夠通過(guò)控制油菜素內(nèi)脂的生物合成并酸和乙烯.CNMHG烯相互協(xié)同,茉莉自然雜志第34卷第4期科技進(jìn)展酸/乙烯依賴的防御反應(yīng)會(huì)受到寄生性病原菌以及植食萄糖超敏感的表型[00-101]。sis1和gin4兩個(gè)葡萄糖不性昆蟲(chóng)的侵害而被誘導(dǎo)激活;水楊酸則往往與茉莉酸/敏感突變體的發(fā)現(xiàn)進(jìn)- -步確定了糖信號(hào)和乙烯信號(hào)的乙烯相互拮抗,水楊酸依賴的防御反應(yīng)主要受到活體營(yíng)拮抗關(guān)系，因?yàn)檫@兩個(gè)突變都是ctr1的等位突變形養(yǎng)的病原菌侵染而激活591-93]。另一方面,乙烯和水楊式101.102]。 雖然sis1 和gin4在萌發(fā)后的發(fā)育過(guò)程中表酸之間也存在協(xié)同關(guān)系。之前的研究發(fā)現(xiàn),在乙烯不敏現(xiàn)出相似的葡萄糖不敏感表型,但是只有g(shù)in4/ctr1 在感的煙草中乙烯對(duì)于由煙草花葉病毒感染誘發(fā)的水楊暗中表現(xiàn)出組成型的三重反應(yīng)表型。如前所述,過(guò)表達(dá)酸依賴的系統(tǒng)獲得性抗性(systemic acquired resistance,EIN2的C末端雖然可以部分恢復(fù)擬南芥光下生長(zhǎng)的幼SAR)發(fā)病是必需的[94]。乙烯可以增強(qiáng)擬南芥對(duì)水楊苗和成株的乙烯反應(yīng)表型,但是在暗中卻仍沒(méi)有三重反酸的反應(yīng),導(dǎo)致水楊酸應(yīng)答標(biāo)志基因PR-1 表達(dá)增應(yīng)表型,說(shuō)明葡萄糖信號(hào)可能影響ETR1和EIN2下游強(qiáng)[95-96]。由此可見(jiàn),乙烯與水楊酸不僅相互拮抗,乙烯的特定乙烯信號(hào)途徑[,100-101]。進(jìn)一步的研究發(fā)現(xiàn),葡還能對(duì)水楊酸誘導(dǎo)的PR-1基因表達(dá)產(chǎn)生協(xié)同效應(yīng),而萄糖可能通過(guò)植物葡萄糖感受蛋白己糖激酶來(lái)促進(jìn)乙.且這一協(xié)同效應(yīng)在乙烯不敏感突變體ein2中被阻斷烯信號(hào)轉(zhuǎn)錄因子EIN3蛋白的降解,這與乙烯促進(jìn)EIN3了,說(shuō)明乙烯對(duì)水楊酸的調(diào)節(jié)依賴于EIN2且需經(jīng)由乙蛋白的穩(wěn)定性恰好相反;另外,ein3突變體表現(xiàn)出葡萄烯信號(hào)途徑[96]。糖超敏感表型,而在擬南芥中轉(zhuǎn)基因過(guò)表達(dá)EIN3蛋白則會(huì)降低植物對(duì)葡萄糖的敏感性[103]。這一結(jié)果說(shuō)明5.8乙烯與光EIN3可能是葡萄糖和乙烯信號(hào)在ETR1和EIN2下游植物的生長(zhǎng)、發(fā)育離不開(kāi)光，人們對(duì)于光信號(hào)在植相互拮抗的一個(gè)節(jié)點(diǎn)。物體內(nèi)的傳導(dǎo)機(jī)制研究由來(lái)已久。如前所述,乙烯處理(2012年2月17日收到)能夠?qū)е乱蕾囉贖LS1的ARF2蛋白水平的降低,進(jìn)而[1 ] JOHNSONP R, ECKERJ R. The ethylene gas signal trans-造成頂端彎鉤兩側(cè)細(xì)胞生長(zhǎng)速率產(chǎn)生差異從而加劇彎duction pathway: a molecular perspective [J]. Annu Rev鉤65.9798]。研究發(fā)現(xiàn)，光和乙烯對(duì)頂端彎鉤的作用恰[2] BLEECKERA B, KENDE H. Ethylene: a gaseous signal mol-好相反,光照能夠引起HLS1蛋白水平降低，進(jìn)而導(dǎo)致ecule in plants [J]. Annu Rev Cell Dev Biol, 2000, 16:1-18.ARF2蛋白積累使彎鉤消除66]。由此看出,光、乙烯和[3] KENDRICK M D, CHANG C. Ethylene signaling: new levelsof complexity and regulation [J]. Curr Opin Plant Biol, 2008,生長(zhǎng)素在控制植物頂端彎鉤形成方面是協(xié)同作用的。11: 479-485.最近的研究發(fā)現(xiàn),乙烯能夠促進(jìn)植物由暗形態(tài)建成到光[ 4] STEPANOVA A N, ECKER J R. Ethylene signaling: from mu-tants to molecules [J]. Curr Opin Plant Biol, 2000, 3:353-360.形態(tài)建成的轉(zhuǎn)換[9]。在植物幼苗中,原葉綠酸(proto-.[5] CHANG C, KWOK SF, BLEECKER A B, MEYEROWITZchlorophyllide, Pchlide) 需經(jīng)過(guò)光依賴的氧化還原酶E M. Arabidopsis cthylenc-response gene ETR1: similarity ofPOR( protochlorophyllide oxidoreductase) 催化形成葉product to two-component regulators [J]. Science， 1993,262: 539-544.綠酸(chlorophyllide, Chlide), 以促進(jìn)葉綠體的形成而[6] HUA J, SAKAI H, NOURIZADEH s, et al. EIN4 and ERS2實(shí)現(xiàn)光形態(tài)建成。黑暗導(dǎo)致的原葉綠酸的過(guò)度積累對(duì)are members of the putative ethylene receptor gene family inArabidopsis [J]. Plant Cell, 1998，10: 1321-1332.植物具有光毒性。研究發(fā)現(xiàn),在黑暗中乙烯信號(hào)可以通.[ 7 ] KIEBER JJ，ROTHENBERG M, ROMANG, etal. CTR1,過(guò)其轉(zhuǎn)錄因子EIN3/EIL1抑制葉綠素前體Pchlide 的a negative regulator of the ethylene response pathway in Ara-過(guò)度積累;另外,EIN3/EIL1可以直接誘導(dǎo)PORA/B基bidopsis, encodes a member of the raf family of protein kina-ses[J]. Cell, 1993，72: 427-441.因的轉(zhuǎn)錄從而促進(jìn)葉綠素合成,從而促進(jìn)了植物由暗形[8] GAO z, CHEN Y F, RANDLETT M D, et al. Localization態(tài)建成到光形態(tài)建成的轉(zhuǎn)換[99]。of the Raf like kinase CTR1 to the endoplasmic reticulum ofArabidopsis through participation in ethylene receptor signa-ling complexes [J]. J Biol Chem, 2003, 278: 34725-34732.5.9乙烯與葡萄糖[9] ALONSOJ M, HIRAYAMA T, ROMANG, etal. EIN2,a .bifunctional transducer of ethylene and stress responses in Ar.葡萄糖不僅作為能量供應(yīng)物質(zhì)存在,它也是植物生abidopsis[J]. Science, 1999, 284: 2148-2152.長(zhǎng)發(fā)育過(guò)程中的重要信號(hào)分子。科學(xué)家在研究葡萄糖[10] CHAO Q, ROTHENBERG M, SOLANO R, et al. Activation不敏感突變體gin1 時(shí)發(fā)現(xiàn)了葡萄糖和乙烯信號(hào)之間相of the ethylene gas response pathway in Arabidopsis by thenuclcar protein ETHYLENEINSENSITIVE3and related pro-互拮抗的關(guān)系[100]。乙烯過(guò)表達(dá)突變體eto1和乙烯組tcins[J]. Cell, 1997, 89: 1133-1144.成型信號(hào)突變體ctr1表現(xiàn)出葡萄糖不敏感的表型強(qiáng)烈∩Q, et al. Nuclear eventsin eth中國(guó)煤_ascade mediated by ETH-支持了這一-拮抗關(guān)系。與此相一致的是,幾個(gè)乙烯不敏YLENGLENE- RESPONSE-FAC.感突變體etr1-1, ein2, ein3 以及ein6 則表現(xiàn)出對(duì)葡TORIYH1 CNM H GUuNEProgressChinese Journal of Nature Vol.34 No. 4[12] BINDER B M，RODRfGUEZ F I, BLEECKER A B. TheBiol Chem, 2004, 279: 48734-48741.Copper Transporter RAN1 Is Essential for Biogenesis of Eth-[29] RODRIGUEZFI, ESCHJJ, HALLAE, etal. A copperylene Receptors in Arabidopsis [J]. J Biol Chem, 2010, 285:cofactor for the ethylene receptor ETR! from Arabidopsis37263-37270.[J]. Science, 1999, 283(5404) : 996-998.[13] RESNICKJS, WENC K, SHOCKEYJ A, et al. REVER.[30] ALONSOJ M, STEPANOVA A N, SOLANOR, et al. FiveSION-TO-ETHYLENE SENSITIVITY1， a conserved genecomponents of the ethylenc-response pathway identified in athat regulates ethylene receptor function in Arabidopsis [J].screen for weak ethylene insensitive mutants in ArabidopsisProc Natl Acad Sci USA, 2006, 103: 7917.7922.[J]. Proc Natl Acad Sci USA, 2003a, 100: 2992-2997.[14] DONG C H, RIVAROLA M, RESNICK JS, et al. Subcellu. .[31] HUAJ, MEYEROWITZ E M. Ethylene responses are nega-lar co-localization of Arabidopsis RTE1 and ETR1 supports atively regulated by a receptor gene family in Arabidopsis thali-regulatory role for RTE1 in ETR1 ethylene signaling [J].ana [J]. Cell, 1998, 94: 261-271.Plant J, 2008, 53: 275-286.[32] HALL A E. BLEECKER A B. Analysis of combinatorial loss[15] GAGNE J M, SMALLE J, GINGERICH D], et al. Arabi-of-function mutants in the Arabidopsis ethylene receptors re-dopsis EIN3-binding F-box 1 and 2 form ubiquitin-protein liga-veals that the ers1etr1 double mutant has severe developmentalses that repress ethylene action and promote growth by direc-defects that are EIN2 dependent [J]. Plant Cell, 2003, 15: .ting EIN3 degradation [J]. Proc Natl Acad Sci USA, 2004 ,2032- 2041.101: 6803-6808.[33] BINDER B M. O'MALLEY RC, WANG w y,etal. Ara-[16] GUO H, ECKERJ R. Plant responses to ethylene gas are me.bidopsis seedling growth response and recovery to ethylene. Adiated by SCF ( EBF1/EBF2 )-dependent proteolysis of EIN3kinetic analysis [J]. Plant Physiol, 2004a, 136; 2913-2920.transcription factor [J]. Cell, 2003, 115; 667-677.[34] XIEF, LIUQ, WEN C K. Receptor signal output mediated[17] POTUSCHAK T, LECHNER E, PARMENTIER Y，et al.by the ETR1 N-terminus is primarily subfamily I receptors-EIN3-dependent regulation of plant ethylene hormone signa-dependent [J. Plant Physiol, 2006，142:492-508.ling by two Arabidopsis F tbox protcins: EBF1 and EBF2 [J].[35] BARRY C s, GIOVANNONI J J. Ripening in the tomatoCell, 2003, 115: 679-689.green-ripe mutant is inhibited by ectopic expression of a pro-[18] QIAO H, CHANG K N, YAZAKIJ, et al. Interplay betweentein that disrupts ethylene signaling []. Proc Natl Acad Scicthylene, ETP1/ETP2 F-box protins, and degradation ofUSA, 2006. 103: 7923-7928.EIN2 triggers cthylene responses in Arabidopsis [J]. Genes &[36] CLARK K L, LARSENP B, WANG X, et al. Association ofDev, 2009, 23:512-521.the Arabidopsis CTR1 Raf-like kinase with the ETR1 and[19] OLMEDO G, GUO H, GREGORY B D, et al. ETHYLENE-ERS ethylene receptors [J]. Proc Natl Acad Sci USA, 1998,INSENSITIVE5 encodes a 5'- +3' exoribonuclease required for95: 5401-5406.regulation of the EIN3-targeting F-box proteins EBF1/2 [J].[37] HUANG Y, LI H, HUTCHISON c E. et al. BiochemicalProc Natl Acad Sci USA, 2006, 103: 13286-13293.and functionalanalysis of CTR1, a protein kinase that nega-[20] POTUSCHAK T, VANSIRI A, BINDER BM,ctal. The ex.tively regulates ethylene signaling in Arabidopsis [J]. PlantJ,oribonuclease XRN4 is a component of the ecthylene response2003, 33: 21-233.pathway in Arabidopsis [J]. Plant Cell, 2006，18:3047-3057.[38] NOVIKOVA G v, MOSHKOV 1E, SMITHAR, etal. The[21] YOOSD, CHO Y H, TENA G, et al. Dual control of nucie-effect of ethylene on MAPKinase-like activity in Arabidopsisar EIN3 by bifurcate MAPK cascades in Cr H4 signaling [J].thaliana [J]. FEBS Lett, 2000, 474: 29-32.Nature, 2008, 451: 789-795.39] OUAKED F，ROZHON w, LECOURIEUx D, et al. A[22]AnF Y, ZhaoQ, Ji Y s, et al. Ethylene- induced stabilizationMAPK pathway mediates ethylene signaling in plants [J].of ETHYLENE INSENSITIVE3 and EIN3-LJKE1 is mediatedEMBOJ, 2003, 22: 1282-1288.by proteasomal degradation of EIN3 binding F-Box 1 and 2[40] ECKER J R. Reentry of the ethylene MPK6 module [J].that requires EIN2 in Arabidopsis [J]. Plant Cell, 2010, 22:Plant Cell, 2004, 16: 3169-3173.2384-2401 .[41] LIU Y, ZHANG s. Phosphorylation of 1-aminocyclopropane.[23] SAKAI H, HUAJ, CHEN Q G, et al. ETR2 is an ETR1-ike1-carbo:)xylic acid synthase by MPK6, a stress-responsive mito-gene involved in ethylene signaling in Arabidopsis [J]. Procgen-activated protein kinase, induces ethylene biosynthesis inNatl Acad Sci USA, 1998, 95; 5812-5817.Arabidopsis [J]. Plant Cell, 2004, 16: 3386-3399.[24] CHANG C, STADLER R. Ethylene hormone receptor action[42] J00 s, LIU Y, LUETH A, et al. MAPK phosphorylation-in.in Arabidopsis [J]. Bioessays, 2001. 23: 619-627.duced stabiliation of ACS6 protein is mediated by the non-[25] SCHALLER G E, BLEECKER A B. Ethyiene binding sitescatalytic C-terminal domain, which also contains the cis-deter-generated in yeast expressing the Arabidopsis ETR1 gene [J].minant for rapid degradation by the 26S proteasome pathwayScience, 1995，270: 1809-1811.[J]. PlantJ, 2008, 54: 129-140.[26] WANG W Y, HALL AE, O'MALLEY R, et al. Canonical[43] XUJ, LI Y, WANG Y, ct al. Activation of MAPK kinase 9histidine kinase activity of the transmitter domain of theinduccs ethylene and camalexin biosynthesis and enhances sen-ETR1 ethylene receptor from Arabidopsis is not required forsitivity to salt stress in Arabidopsis [J]. J Biol Chem, 2008,signal transmission [J]. Proc Natl Acad Sci USA, 2003, 100:283: 26996-27006.[44] BETHKE G, UNTHAN T, UHRIGJF, et al. Flg22 regu-[27] GAMBLE R L. QU X, SCHALLER G E. Mutational analysislates the release of an ethylene response factor substrate fromof the ethylene receptor ETR1. Role of the histidine kinaseMAP kinase 6 in Arabidopsis thaliana via ethylene signalingdomain in dominant ethylene insensitivity [J]. Plant Physiol,[J]. Proc Natl AcadLSei USA.2009. 106: 8067-8072.2002，128: 1428-1438.[45] GUZM中國(guó)煤化工triple responseof Ar-[28] MOUSSATCHE P, KLEE H J. Altophosphorylation activityabidopsCNMH Glians[J]. Plan Cll.of the Arabidopsis ethylene receptor multigene family [J]. J1990 ,YH●226●自然雜志第34卷第4期科技進(jìn)展.[46] BISSON M M，BLECKMANN A, ALlEKOTTE s, et al.[64] ABEL s, NGUYEN M D, CHOW w, et al. ASC4, a primaryEIN2, the central regulator of ethylene sigalling. is localizedindoleacetic acid-responsive gene encoding 1-aminocyelopro-at the ER membrane where it interacts with the ethylene re-pane- 1-carboxylate synthase in Arabidopsis thaliana : structur-ceptor ETR1 [J]. BiochemJ, 2009, 424(1): 1-6.al charactcrization, expression in Escherichia coli, and ex-[47] CHRISTIANS MJ, ROBLES L M, ZELLERSM, etal. Thepression characteristics in response to auxin [J]. J Biol Chem,eer5 mutation, which affects a novel proteasome-related sub-1995，270: 19093-19099.unit, indicates a prominent role for the COP9 signalosome in[65] LEHMAN A, BLACK R, ECKERJ R. HOOKLESS1. an ethyl-resetting the ethylene-signaling pathway in Arabidopsis [J]. .cne response gene, is required for differential cell elongation in thePlant J, 2008，55; 467-477.Arabidopsis hypocotyl [J]. Cell, 1996, 85; 183-194.[48] BISSON M M, GROTH G. New insight in ethylene signaling:[66] LI H, JOHNSON P, STEPANOVA A, et al. Convergence ofautokinase activity of ETR1 modulates the interaction of re-signaling pathways in the control of differential cell growth inceptors and EIN2 [J]. Mol Plant, 2010, 3: 882-889 .Arabidopsis [J]. Dev Cell, 2004, 7: 193-204.[49] FUJITA H, SYONO K. Genetic analysis of the effects of po-[67] WOESTE K E, YE c, KIEBER JJ. Two Arabidopsis mutantslar auxin transport inhibitors on root growth in Arabidopsisthat overproduce ethylene are affected in the posttranscrip-thaliana [J]. Plant Cell Physiol, 1996, 37; 1094-1101.tional regulation of 1-aminocyclopropane-1-carboxylic acid[50]SU w P, HOWELLS H. A single genetic locus, Ckrl, de-synthase [J]. Plant Physiol, 1999, 119: 521-530.fines Arabidopsis mutants in which root growth is resistant to68] ARTECA R N, ARTECA了M. Effects of brassinosteroid,low concentrations of cytokinin [J]. Plant Physiol, 1992, 99:auxin, and cytokinin on ethylene production in Arabidopsis1569-1574.thaliana plants [J]. J Exp Bot, 2008. 59; 3019-3026.[51] BINDER B M，MORTIMORE L A. STEPANOVA A N, et[69] VOGELJ P, WOESTE K E, THEOLOGIS A, et al. Reces-al. Short-term growth responses to ethylene in Arabidopsissive and dominant mutations in the ethylene biosynthetic geneseedlings are EIN3/EIL1 independent [J]. Plant Physiol,ACS5 of Arabidopsis confer cytokinin insensitivity and ethyl-2004，136; 2921-2927.ene overproduction, respectively []]. Proc Natl Acad Sci[52] OHME-TAKAGI M, SHINSHI H. Ethylene-inducible DNAUSA, 1998, 95: 4766-4771.binding proteins that interact with an ethylene responsive elc-[70] CHAE H s, FAURE F, KIEBERJ J. The elo1, elo2, andment [J]. Plant Cell, 1995, 7: 173-182.e1o3 mutations and cytokinin treatment increase ethylene bio-[53] ALONSOJ M, STEPANOVA A N, LEISSE T J, et al. Ge-synthesis in Arabidopsis by increasing the stability of ACSnome-wide insertional mutagenesis of Arabidopsis thalianaprotein []. Plant Cell, 2003, 15: 545-559.[J]. Science, 2003b, 301: 653-657.[71] HANSEN M，CHAE H s. KIEBER J J. The regulation of[54] STEPANOVA A N, ALONSOJ M. Ethylene signaling and re-ACS protein stability by cytokinin and brassinosteroid [J].sponsc: where different regulatory modules meet [J]. CurrPlant J, 2009, 57: 606-614.Opin Plant Biol, 2009，12: 548-555[72] CALVOA P, NICOLAS C, NICOLAS G, et al. Evidence of[55] STEPANOVA A N, ALONSOJ M. Ethylene signaling and re-a cross-talk regulation of a GA 20-oxidase ( FsGA20ox1) bysponse pathway: A unique signaling cascade with a multitude of in-gibberellins and ethylene during the breaking of dormancy inputs and outputs [J]. Plant Physiol, 2005， 123: 195-206.Fagus sylvaica seeds [J]. Physiol Plantarum, 2004. 120: 623-[56] ROMAN G, LUBARSKY B, KIEBER J J, et al. Genetic630.analysis of ethylene signal transduction in Arabidopsis thali-[73] HIRANO K，UEGUCHI-TANAKA M，MATSUOKA M.ana: five novel mutant loci integrated into a stress responseGID1-mediated gibbrellin signaling in plants [J]. Trendspathway [J]. Genetics, 1995, 139: 1393-1409.Plant Sci, 2008, 13; 192-199.[57] BENNETT M J, MARCHANT A. GREENHG, etal. Ara-[74] ACHARD P, VRIEZEN w H, VAN DER STRAETEN D, etbidopsis AUX1 gene: a permease-like regulator of root grav.al. Ethylene regulates Arabidopsis development via the modu-itropism [J]. Science, 1996, 273: 948-950.lation of DELLA protein growth repressor function [J]. Plant[58] BARTEL B. Auxin biosenthesis [J]. Annu Rev Plant PhysiolCell, 2003, 15: 2816-2825.Plant Mol Biol, 1997, 48: 51-66.[75] ACHARD P, BAGHOUR M, CHAPPLE A. et al. The plant[59] STEPANOVA A N, HOYTJ M, HAMILTONAA,etal. Astress hormone ethylene controls floral transition via DELLA-link between ethylene and auxin uncovered by the character.dependent regulation of floral meristem-identity genes [J].ization of two root specific ethylene-insensitive mutants in Ar-Proc Natl Acad Sci USA, 2007, 104 : 6484-6489.abidopsis [J]. Plant Cll, 2005, 17: 2230-2242.[76] AN F, ZHANG X, ZHU z, et al. Coordinated regulation of[60] STEPANOVA A N, ROBERTSON-HOYT J, YUN J, et al.apical hook development by gibbrellins and ethylene in etio-TAA 1-mediated auxin biosynthesis is essential for hormonelated Arabidopsis seedlings [J]. Cell Res, 2012, 22: 915-927.crosstalk and plant development [J]. Cell, 2008, 133: 177-191.[77] GHASSEMIAN M, NAMBARA E, cutlers, et al. Regu-[61] RUZICKA K, LJUNG K, VANNESTE S, et al. Ethylene .lation of abscisic acid signaling by the ethylene response path-regulates root growth through effects on auxin biosynthesisway in Arabidopsis [J]. Plant Cell, 2000, 12: 117-1126.and transport-dependent auxin distribution [J]. Plant Cell,[78] BEAUDOIN N, SERIZET c, GOSTI F, et al. Interactions2007, 19: 2197-2212.between abscisic acid and ethylene signaling cascades [J}.[62] STEPANOVA A N, YUN J, LIKHACHEVA A V, et al.Plant Cell, 2000, 12: 1103-1115.Multilevel interactions between ethylene and auxin in Arabi-[79] TANAKA Y, SANO T, TAMAOKI M, et al. Ethylene inhib-dopsis roots [J]. Plant Cell, 2007， 19: 2169-2185 .its abscisic acid- induced stomatal closure in Arabidopsis [J].[63] SWARUP R, PERRY P, HAGENBEEK D, et al. EthylenePlantupregulates auxin biosynthesis in Arabidopsis seedlings to en-[80] DE中國(guó)煤化工EtIEtzo, etal.hance inhibition of root cell elongation [J]. Plant Cell, 2007,AuxirYHCN M H G; tipartite control of19; 2186-2196.growi2J]. Plant Cell Physiol,●227●ProgressChinese Journal of Nature Vol. 34 No. 42005, 46(6): 827-836.[100] ZHOU L. JANG JC, JONES T L. et al. Glucose and ethyl-[81] GENDRONJ M, HAQUEB A, GENDRONBN, et al. Chem.ene signal transduction crosstalk revealed by an Arabidopsisical genetic disection of brassinostcroid-ethylene interactionglucose-insensitive mutant [J]. Proc Natl Acad Sci USA.[J]. Mol Plant, 2008, 1(2) : 368-379.1998, 95: 10294.10299.[82] DESLAURIERS S D, LARSEN P B. FERONIA is a key mod-[101] CHENG w H, ENDO A, ZHOU L, et al. A unique short-ulator of brassinosteroid and ethylene responsiveness in Arabi-chain dehydrogenase/ reductase in Arabidopsis glucose signa-dopsis hypocotyls [J]. Mol Plant, 2010, 3(3) : 626-640.ling and abscisic acid biosynthesis and functions [J]. Plant[83] MEMELINK J. Regulation of gene expression by jasmonateCell, 2002. 14: 2723-2743.hormoncs [J]. Phytochemistry, 2009, 70; 1560-1570.[102] GIBSON s I, LABY R J, KIM D. The sugar. insensitive1[84] TURNERJ G, ELLIS C E, DEVOTO A. The jasmonate sig-(sis1) mutant of Arabidopsis is alelie to cIr1 [J]. Biochemnal pathway [J]. Plant Cell, 2002, 14: s153-S164.Bioph Res Co, 2001, 280; 196-203.[85] BERROCAL-LOBO M，MOLINA A. Ethylene response fac-[103] YANAGISAWA s, Y00 s D, SHEEN J. Differential regu.tor 1 mediates Arabidopsis resistance to the soilborne funguslation of EIN3 stability by glucose and ethylene signalling inFusarium oxysporum [J]. Mol Plant Microbe Interact, 2004,plants [J]. Nature, 2003, 425: 521-525.17: 763-770.[86] DONG X N. SA, JA, ethylene, and disease resistance inplants [J]. Curr Opin Plant Biol, 1998， 1(4): 316-323.Study of Ethylene Signal Transduction Pathway[87] BROWN R L, KAZAN K, MCGRATH K C, et al. A roleZHANG Cun-li$，GUO Hong-wei@for the GCC-box in jasmonate mediated activation of thePDF1.2 gene of Arabidopsis [J]. Plant Physiol, 2003, 132:①Ph. D. Candidate，②Professor，State Key Laboratory of Protein1020-1032.and Plant Gene Research，School of Life Sciences，Peking Universi-[88] LORENZO o, PIQUERAS R, SANCHEZ-SERRANOJ J,ly, Beijing 100871. ChinaSOLANO R. ETHYLENE RESPONSE FACTOR1 integratesAbstract As one of the five classical phytohormones, ethylene hassignals from ethylene and jasmonate pathways in plant defense[J]. Plant Cell, 2003，15: 165-178.very simple structure, the gascous phytohormone ethylene has im-[89] PENNINCKXI, EGGERMONT K，TERRAS F, et al.portant effects on the developmental processes and stress responsesPathogen-induced systemic activation of a plant defensin geneof plant. Through nearly two decades of research, scientists estab-in Arabidopsis follows a salicylic acid- independent pathwaylished a largely linear ethylene signal transduction pathway. In the[J]. Plant Cell, 1996, 8: 2309-2323.[90] ZHUz, AN F, FENG Y, et al. Derepression of ethylene-model plant Arabidopsis, there are five ethylene receptors ETR1,stabilized transcription factors ( EIN3/ELL1) mediates jas-ETR2, ERS1, ERS2 and EIN4 encoded by a multigene family inmonate and ethylene signaling synergy in Arabidopsis [J ].the upstream of this signaling pathway. A Raf-like protein kinaseProc Natl Acad Sci USA, 2011, 108(30): 12539-12544.CTR1 combines with ethylene receptors and co-localizes in the ER[91] KESSLER A, BALDWIN I T. Plant responses to insect her-membrane together with these receptors. In the absence of ethyl-bivory: the emerging molecular analysis [J]. Annu Rev Plantene, receptors and CTR1 can inhibit the downstream ethylene sig-Biol, 2002, 53: 299-328.naling together. A positive regulator EIN2 is the downstream of[92] GLAZEBROOK J. Contrasting mechanisms of defense againstthese two negative regulators. If EIN2 gene is mutated, the etiola-biotrophic and necrotrophic pathogens [J]. Annu Rev Phyto-ted seedlings of plant will show completely ethylenc insensitive phe-pathol, 2005, 43; 205-227.notype even when high concentration of ethylene exists, which[93] HOWE G A, JANDER G. Plant immunity to insect herbi-demonstrates that EIN2 plays a key role in ethylene signaling path.vores [J]. Annu Rev Plant Biol, 2008, 59: 41-66.[94] VERBERNE M C, HOEKSTRAJ, BOLJ F, et al. Signalingway. EIN3 and EILs are transcription factors downstream of EIN2.of systemic acquired resistance in tobacco depends on ethyleneThey will start the transcription of ethylene related genes in re-sponse to ethylene signal. It was also found that these transcriptionperception [J]. Plant J, 2003, 35: 27-32.[95] LAWTON K A, POTTER s L, UKNES s, et al. Acquired re-factors were regulated by ubiquitin/ proteasome degradation path-sistance signal transduction in Arabidopsis is ethylene inde-way. The F-box proteins, which are responsible for recognition andpendent [J]. Plant Cell, 1994, 6; 581-588.[96] DE vos M，VAN ZAANEN w, KOORNNEEF A, et ai.3’exonuclease and antagonizes the negative feedback regulation onHerbivore-induced resistance against microbial pathogens inEIN3 by promoting EBFI and EBF2 mRNA decay. Recently, stud-Arabidopsis [J]. Plant Physiol, 2006， 142: 352-363.ies have shown that EIN2 is also a short hal-life protein and will be[97] sILK W H, ERICKSON R o. Kinematics of hypocotyl curva-degraded by the ubiquitin/ proteasome pathway. Another two F-boxture[J]. Am J Bot,1978, 65: 310-319.proteins ETP1 and ETP2 are responsible for the regulation of EIN2[98] HARPHAMN VJ, BERRY A w, KNEEEM, et al. Theprotein. Although grcat progress was made in ethylene signal trans-effect of ethylene on the growth and development of wide-athway, further research on the fine-tuning of ethylenetype and mutant Arabidopsis thaliana (L.) Heynh [J]. Annsignal transduction and the crosstalk between ethylene and otherBot (Lond), 1991,68: 55-61.[99] ZHONG s, ZHAO M, SHI T, et al. EIN3/EIL1 cooperatephytohormones still need to be detected.with PIF1 to prevent photo-oxidation and to promote greeningKey words phytohormone, ethylene ，signal transductionof Arabidopsis seedlings [J]. Proc Natl Acad Sci USA, 2009,106: 21431-21436.中國(guó)煤化工(編輯: 沈美芳)YHCNMHG