十字花科植物抗根腫病研究進(jìn)展

張 凡， 李林梅， 崔海芳， 尹俊龍， 郭英琪， 岳艷玲*

(1.云南農(nóng)業(yè)大學(xué) 園林園藝學(xué)院，云南 昆明 650201；2.中國(guó)科學(xué)院 昆明動(dòng)物研究所，云南 昆明 650000)

十字花科植物抗根腫病研究進(jìn)展

張 凡1， 李林梅1， 崔海芳1， 尹俊龍1， 郭英琪2， 岳艷玲1*

(1.云南農(nóng)業(yè)大學(xué) 園林園藝學(xué)院，云南 昆明 650201；2.中國(guó)科學(xué)院 昆明動(dòng)物研究所，云南 昆明 650000)

十字花科植物根腫病是由根腫菌侵染而引起的一種危害極大的世界性土傳病害.近年來，該病在我國(guó)多個(gè)地區(qū)迅速蔓延，危害十分嚴(yán)重，制約著我國(guó)十字花科作物產(chǎn)業(yè)的發(fā)展.根腫病的抗病研究已經(jīng)成為國(guó)內(nèi)外學(xué)者研究的熱點(diǎn).根據(jù)近年來根腫菌研究的最新研究進(jìn)展和結(jié)果，總結(jié)了根腫菌在侵染過程中寄主植物的抗根腫病信號(hào)傳導(dǎo)途徑，抗病基因和遺傳機(jī)制，深入探討了抗根腫病研究過程中存在的主要問題，以期為未來根腫病抗病研究提供理論參考和研究思路.參47.

根腫?。簧硇》N；抗病基因;育種；十字花科

十字花科根腫病是由根腫菌(Plasmodiophorabrassicae)引起的十字花科植物根系病，現(xiàn)已成為全球十字花科作物中最嚴(yán)重的疾病之一[1].根腫病菌病原體能夠侵染危害100多種十字花科植物[2]，并且在土壤中存活多達(dá)20年[3].迄今為止，十字花科根腫病的危害可使我國(guó)十字花科作物的產(chǎn)量損失約達(dá)25%，而病情嚴(yán)重的地區(qū)，其產(chǎn)量損失可達(dá)60%[4]，十字花科根腫病給我國(guó)帶來了巨大的經(jīng)濟(jì)損失[5].

許多傳統(tǒng)的栽培管理措施以及生物防治，包括殺真菌劑的應(yīng)用對(duì)其都無效[6-8]，遺傳育種無疑是最有效和最經(jīng)濟(jì)的方法.為此，針對(duì)近年來在十字花科植物抗根腫病研究方面取得的新成果、新技術(shù)進(jìn)行綜述，以期為十字花科作物抗根腫病育種提供理論參考.

1 抗根腫病基因

1981年，Yoshikawa在源于歐洲的飼用蕪菁中找到了具有高度抗性的CR基因[9].迄今為止，世界上公認(rèn)的抗根腫病基因有8個(gè)，分別是Crr1、Crr2、Crr3、Crr4、CRa、CRb、CRc 和CRk[10]，隨后也有人發(fā)現(xiàn)新的抗病基因PbBa3.1和PbBa3.3[11]，其中人們對(duì)CRb的關(guān)注度較高，認(rèn)為它是抗大白菜根腫病最重要的基因.也有人提出CRa與CRb可能是等位基因或者緊密連鎖兩個(gè)抗病位點(diǎn)[12]，但趙卓在他的研究中證明了CRa與CRb不是等位基因[13].Teng Zhang結(jié)合群體分離分析法和生物信息學(xué)分析對(duì)CRb進(jìn)行精確定位，確定CRb、CRa和CRbKato是緊密連鎖的[14].Saito等通過與擬南芥進(jìn)行比較，精細(xì)定位了Crr3基因，且證明Crr3與CRb不是同一位點(diǎn)[15].這些研究結(jié)果為CRb基因的分離提供了有用的信息，并為十字花科抗病育種基因的緊密連鎖提供了一定的技術(shù)手段.

2 抗根腫病信號(hào)轉(zhuǎn)導(dǎo)途徑

Chen等在2015年通過對(duì)大白菜抗感近等基因系根的RNA測(cè)序完成其轉(zhuǎn)錄圖譜，共檢測(cè)出42 730個(gè)基因，發(fā)現(xiàn)上調(diào)基因1 875個(gè)，下調(diào)基因2 013個(gè).而在所有植物-病原體互作有關(guān)的基因中，有151個(gè)基因在抗感近等基因系中表現(xiàn)出不同的表達(dá)模式，涉及PAMP、效應(yīng)識(shí)別、鈣離子內(nèi)流、激素信號(hào)、轉(zhuǎn)錄因子和細(xì)胞壁修飾等途徑和過程.其中，激素信號(hào)傳導(dǎo)途徑應(yīng)用最多的當(dāng)屬水楊酸(SA)、茉莉酸(JA)和乙烯(ET).[16]SA信號(hào)傳導(dǎo)主要依賴于NPR1，其在休眠細(xì)胞中作為寡聚體被隔離在細(xì)胞質(zhì)中.在這種情況下，只有少量的NPR1單體轉(zhuǎn)移到細(xì)胞核內(nèi)，并被NPR1的旁系同源物NPR3和NPR4泛素化和降解[17].增加SA水平可誘導(dǎo)細(xì)胞氧化還原平衡的改變，從而釋放大量的NPR1單體，這些NPR1單體進(jìn)入細(xì)胞核后，除少量被泛素化和降解外，大多數(shù)都與SA結(jié)合，誘導(dǎo)NPR1 C-末端結(jié)構(gòu)域的構(gòu)象變化[18]，使其與TGA轉(zhuǎn)錄因子家族的成員相互作用，從而促進(jìn)防御相關(guān)基因PR1和WRKY等的轉(zhuǎn)錄激活[19].

在非誘導(dǎo)細(xì)胞中，JAZ蛋白通過其與轉(zhuǎn)錄因子MYC2/3/4的相互作用而作為轉(zhuǎn)錄抑制子[20].NINJA銜接蛋白充當(dāng)支架，并介導(dǎo)JAZ蛋白與共抑制物TPL的相互作用，防止JA相關(guān)基因表達(dá)的不適時(shí)活化[21].而在受到JA “攻擊”的細(xì)胞中，JA被COI1-JAZ受體復(fù)合物感知[22].致使NINJA、JAZ、MYC2/3/4、TPL復(fù)合體解體并使JAZ泛素化，從而釋放出MYC轉(zhuǎn)錄因子，激活JA[22].在沒有ET的情況下，CTR1能夠在內(nèi)質(zhì)網(wǎng)膜中與ET受體ETR1相互作用，使EIN2磷酸化，阻止其進(jìn)入細(xì)胞核內(nèi)[23].在細(xì)胞核內(nèi)的轉(zhuǎn)錄激活因子EIN3被蛋白酶體降解，阻止ET信號(hào)的活化[24].而在ET存在的情況下，ET與ETR1受體結(jié)合，導(dǎo)致CTR1失活，阻止EIN2磷酸化[23].未磷酸化的EIN2經(jīng)歷蛋白水解切割，進(jìn)入細(xì)胞核內(nèi)，進(jìn)入細(xì)胞核內(nèi)的EIN2抑制EIN3的蛋白酶體降解，從而觸發(fā)ET信號(hào)傳導(dǎo)[23,24].

在擬南芥的休眠細(xì)胞中，WRKY33在與含有VQ基序的MKS1和MPK4復(fù)合物中活性受到抑制[25].但在植物感知病原體時(shí)，MAPK4將MKS1磷酸化，磷酸化的MKS1與WRKY33相互作用，能夠激活植物抗毒素—camalexin的轉(zhuǎn)錄[25].MPK3/MPK6將WRKY33磷酸化是camalexin生物合成和激活WRKY33本身轉(zhuǎn)錄所必需的，這形成了正反饋調(diào)節(jié)環(huán)[26].被MPK3/MPK6磷酸化的WRKY33與含VQ的基序蛋白SIB1/2的相互作用可刺激其DNA結(jié)合活性，從而促進(jìn)防御反應(yīng)[27].在葡萄休眠細(xì)胞中，WRKY1 / 2抑制防御基因表達(dá)[28]，并阻礙MYB6激活防御反應(yīng)[29].在植物感知病原體后，R蛋白MLA10被激活并與WRKY1/2相互作用，從而通過WRKY1抑制釋放HvMYB6[28,29].釋放的HvMYB6可以直接與MLA6的相互作用激活防御基因表達(dá)[29].MLA在細(xì)胞質(zhì)和細(xì)胞核中都能有效的激活防御信號(hào)，在細(xì)胞質(zhì)中可使細(xì)胞程序性死亡，而在細(xì)胞核中可限制真菌生長(zhǎng)[30].

在休眠細(xì)胞中，阻遏物SRFR1在內(nèi)膜上與EDS1和無活性的RPS4和RPS6R蛋白相互作用[31,32].效應(yīng)物AvrRps4和HopA1與EDS1的相互作用導(dǎo)致駐留在內(nèi)膜上的受體復(fù)合物的擾動(dòng)[29].釋放的RPS4-EDS1-AvrRPS4信號(hào)轉(zhuǎn)導(dǎo)復(fù)合物的分子活性的胞質(zhì)協(xié)調(diào)是激活細(xì)胞質(zhì)細(xì)胞死亡和防御基因的轉(zhuǎn)錄激活所必需的，而核RPS4-EDS1-AvrRPS4復(fù)合物限制細(xì)菌生長(zhǎng)[33].R蛋白SNC1通過其與轉(zhuǎn)錄共抑制蛋白的相互作用促成RPS4防御反應(yīng)[34].

3 根腫病抗病育種

3.1 生理小種鑒定

根腫病主要是由根腫菌侵染引起的土傳性病害，而根腫菌又存在小種分化[35].目前，利用生理小種鑒別系統(tǒng)已先后發(fā)現(xiàn)13種生理小種，現(xiàn)在用于根腫病生理小種鑒定的方法主要有兩種，一種為Williams鑒定系統(tǒng)，該鑒別系統(tǒng)由4個(gè)十字花科蕓薹屬植物(2個(gè)結(jié)球甘藍(lán)品種Jerseyqueen、BadgerShipper；2個(gè)蕪菁甘藍(lán)品種Laurentian、Wilhelmburger)作為鑒別寄主[36]；另一種為歐洲根腫菌生理小種鑒別系統(tǒng)(EDC)，該鑒別系統(tǒng)具有15個(gè)鑒別寄主.而這兩種鑒別系統(tǒng)都具有自身的優(yōu)點(diǎn)和缺點(diǎn).Williams鑒定系統(tǒng)雖然具有鑒別寄主容易、方法易操作的特點(diǎn)，但由于該鑒別系統(tǒng)的鑒別寄主少，對(duì)個(gè)別生理小種或由多個(gè)根腫菌生理小種混合侵染的菌樣，根本無法進(jìn)行明確鑒定.EDC系統(tǒng)寄主繁殖困難，方法繁復(fù)，而且存在地域性—比較適用于歐洲根腫菌菌系的鑒定，不適用亞洲菌系的鑒定.

3.2 抗病性遺傳

弄清楚根腫病的抗性遺傳規(guī)律，是十字花科抗根腫病育種的基礎(chǔ).目前發(fā)現(xiàn)，十字花科不同種屬對(duì)根腫病的抗性不盡相同，甘藍(lán)類要比白菜類抗性高.關(guān)于抗性遺傳規(guī)律研究方面，觀點(diǎn)也不盡相同.根據(jù)J.D.Vriesenga等的研究可知，甘藍(lán)對(duì)根腫病的抗性主要受一個(gè)隱性基因和一個(gè)不完全顯性基因控制[37].在Roeoland E等對(duì)甘藍(lán)根腫病抗性遺傳的研究中也顯示：在所研究的4種抗性遺傳中，一種抗性主要受一對(duì)互補(bǔ)基因控制；還有兩種抗性可能受兩個(gè)基因控制；最后一種抗性是受兩個(gè)以上的基因控制[38].用青花菜與蕓薹屬野生種B2013進(jìn)行雜交，通過對(duì)其進(jìn)行根腫病抗性遺傳規(guī)律研究，發(fā)現(xiàn)其抗病性受2對(duì)基因控制[39].而在對(duì)大白菜的研究中發(fā)現(xiàn),其抗根腫病屬于質(zhì)量遺傳而非數(shù)量遺傳，并由一對(duì)顯性核基因控制.研究表明：抗病純系的基因型為RR；感病純系的基因型為rr；雜合抗性為Rr[ 40].

不同的生理小種抗性遺傳機(jī)制也不同[41].Chiaug對(duì)歐洲油菜的研究發(fā)現(xiàn)，1號(hào)和3號(hào)生理小種的抗性受單一的顯性基因控制，而5號(hào)生理小種的抗性則受兩個(gè)隱性基因控制[42].Standbery通過對(duì)中國(guó)大白菜的研究發(fā)現(xiàn)，中國(guó)大白菜中具有對(duì)6號(hào)和7號(hào)生理小種的抗性，且受顯性基因控制[43].

3.3 抗病品種選育

與國(guó)外相比，國(guó)內(nèi)對(duì)抗根腫病的研究較晚.日本的吉川等人早在1977年就將抗病蕪菁中的抗根腫病基因轉(zhuǎn)育到結(jié)球白菜上，培育出了抗根腫病的結(jié)球白菜.

徐學(xué)忠等人通過多年實(shí)驗(yàn)研究培育出新品種CCR11242.新品種以“綠半白”和韓國(guó)抗根腫病品種“白菜王”為試材，通過小孢子培養(yǎng)，回交，自交等技術(shù)成功育成不育系CCR11239和保持系CCR11240.保持系CCR11240與韓國(guó)品種“白菜王”與魯春白l號(hào)(83-1)經(jīng)過先雜交后自交獲得自交親和系CCR11241進(jìn)行雜交，獲得新品種CCR11242.[44]

張敬文等人利用從韓國(guó)引進(jìn)的抗根腫病品種與高抗病毒病品種9395雜交，經(jīng)4代分離純化，選育出的抗根腫病的自交不親和系：08-5-1；再利用從日本引進(jìn)的抗根腫病品種中自交分離，選育出的自交不親和系：07-8-9.最后將兩個(gè)自交不親和系雜交，育成抗根腫病的新品種CR589.[45]

聶凱采用回交轉(zhuǎn)育模式進(jìn)行抗病品種轉(zhuǎn)育，最終育成抗根腫病雄性不育甲型“兩用系”和臨時(shí)保持系[46].而耿新翠在聶凱的研究基礎(chǔ)上進(jìn)行轉(zhuǎn)育，再經(jīng)過雜交重組、自交、兄妹交、測(cè)交后，成功育成抗根腫病桔紅心大白菜核基因雄性不育系.[47]

4 展 望

根腫病在十字花科植物中的危害日益嚴(yán)重，防治根腫病勢(shì)在必行，而抗病品種的選育無疑是最為安全而又經(jīng)濟(jì)有效的一種方法.但目前為止，雖然研究人員在選育抗根腫病品種這一方面有所收獲，但在實(shí)際推廣運(yùn)用上卻收效甚微.主要原因有以下幾點(diǎn)：(1)生理小種的分化，生理小種經(jīng)過多年不斷的演變，可能會(huì)演變成另一種生理小種，使原來的抗根腫病品種不在對(duì)其具有抗性.這就要求我們要不斷的挖掘新的抗病基因以應(yīng)變生理小種將來的轉(zhuǎn)變.(2)對(duì)地區(qū)生理小種鑒別的不準(zhǔn)確.當(dāng)一個(gè)地區(qū)的菌樣出現(xiàn)幾個(gè)生理小種混生的情況時(shí)，就目前國(guó)際上通用的兩種致病性分化鑒定系統(tǒng)——Williams 系統(tǒng)和European Clubroot Differential Set(ECD) 系統(tǒng)可能會(huì)將優(yōu)勢(shì)種群錯(cuò)判為生理小種.這兩個(gè)鑒定系統(tǒng)除了上述情況外，還存在鑒別條件較難控制等問題.所以我們需要建立一個(gè)完善的鑒別系統(tǒng)來解決這些問題.(3)不同的生理小種其遺傳規(guī)律也不盡相同.由于生理小種的遺傳規(guī)律不同，給抗根腫病育造成了困難，也在生產(chǎn)上產(chǎn)生了阻礙，所以我們不能采取單一的解決方法，需要針對(duì)不同的遺傳機(jī)制進(jìn)行有目的的研究，深入探索調(diào)控遺傳規(guī)律的關(guān)鍵因素，以期為抗根腫病品種選育提供行之有效的理論參考.

[2] Ronald J.Howard,Stephen E.,et al.Harding.Clubroot ofcruciferouscrops: new perspectives on an old disease[J].Canadian Journal of Plant Pathology,2010,32(1):43-57.

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Abstract：Crucifer clubroot caused byPlasmodiophorabrassicaeis a worldwide soil-borne diseases with great harm,which expanded rapidly in many regions of China in recent years and did great harm to the development of industry of cruciferous crop.Researches on clubroot-resistance has been a hot topic at home and abroad.Based on the latest research progress and results ofPlasmodiophorabrassicae,the signal transduction pathway of host plants,resistant genes and genetic mechanism related clubroot resistance were summarized,and the main problems in clubroot resistance research process were deeply discussed in order to provide theoretical reference and ideas for future research on clubroot resistance.47refs.

Keywords：clubroot;Plasmodiophorabrassicaeraces; resistant gene; breeding;Cruciferae

Biography：ZHANG Fan,female,born in 1991,master,research direction: vegetable breeding.

CurrentResearchofCruciferClubrootResistance

ZHANGFan1，LILin-mei1，CUIHai-fang1，YINJun-long1，GUOYing-qi2，YUEYan-ling1*

(1.College of Landscape and Horticulture,Yunnan Agricultural University,Kunming,650201,Yunnan,China;2.Kunming Institute of Zoology.CSA ,Kunming,650000,Yunnan,China)

S63

A

2017-07-12

公益性行業(yè)(農(nóng)業(yè))科研專項(xiàng)(編號(hào)：201003029)；云南農(nóng)業(yè)大學(xué)2016年研究生科技創(chuàng)新項(xiàng)目(編號(hào)：2016ykc34)

張凡(1991-)，女，河南焦作人，碩士研究生，研究方向：蔬菜遺傳育種.

*通訊作者，E-mail: yanling-yue@126.com.注：李林梅為并列第一作者

10.3969/j.issn.2095-7300.2017.03-057