玉米籽粒形成的分子生物學(xué)基礎(chǔ)

2019-11-07 07:45:22趙然蔡曼君杜艷芳張祖新

中國(guó)農(nóng)業(yè)科學(xué) 2019年20期

趙然，蔡曼君，杜艷芳，張祖新

趙然，蔡曼君，杜艷芳，張祖新

（華中農(nóng)業(yè)大學(xué)作物遺傳改良國(guó)家重點(diǎn)實(shí)驗(yàn)室，武漢 430070）

玉米單穗籽粒產(chǎn)量由穗粒數(shù)和粒重兩因子組成。單個(gè)果穗上所著生的籽粒數(shù)與雌花序建成和小花分化密切相關(guān)，因此，控制花序形態(tài)建成和小花發(fā)育的基因可能直接或間接地參與穗粒數(shù)調(diào)控。玉米成熟籽粒主要由源于母本組織的種皮和經(jīng)雙受精產(chǎn)生的胚和胚乳組成，且胚和胚乳占成熟籽粒的絕大部分，直接影響粒重。文中主要從“CLAVATA（CLV）-WUSCHEL（WUS）負(fù)反饋調(diào)控途徑、激素及其信號(hào)途徑、花器官發(fā)育和小花性別決定”等方面總結(jié)了花序和小花發(fā)育相關(guān)基因及其與穗粒數(shù)的關(guān)系，描述了CLV-WUS途徑中各基因在玉米雌花序上特異性表達(dá)的分生組織和基因間的調(diào)控關(guān)系，總結(jié)了生長(zhǎng)素、赤霉素、細(xì)胞分裂素和獨(dú)腳金內(nèi)酯等植物激素的相互作用網(wǎng)絡(luò)，以及已克隆的玉米花器官發(fā)育相關(guān)基因及其功能。從“線粒體基因轉(zhuǎn)錄本的加工和編輯、質(zhì)體基因的轉(zhuǎn)錄和翻譯及細(xì)胞核RNA轉(zhuǎn)錄與加工”3個(gè)方面總結(jié)了已克隆的影響胚和胚乳發(fā)育的相關(guān)基因，其中，大部分基因編碼線粒體或質(zhì)體定位的PPR蛋白。值得關(guān)注的是，近年來(lái)，研究發(fā)現(xiàn)了通過(guò)調(diào)節(jié)細(xì)胞核內(nèi)RNA轉(zhuǎn)錄和加工而影響玉米籽粒發(fā)育的新途徑。文章作者在基因水平上對(duì)玉米籽粒形成的分子生物學(xué)基礎(chǔ)進(jìn)行了簡(jiǎn)要總結(jié)，為進(jìn)一步深入解析玉米產(chǎn)量形成的分子調(diào)控網(wǎng)絡(luò)提供參考。同時(shí)，也就該研究領(lǐng)域今后可能的研究方向進(jìn)行了討論。

玉米；穗粒數(shù)；粒重；花序；小花；胚；胚乳

0 引言

玉米（s L.）籽粒是重要的糧食、飼料、工業(yè)和能源原料，在保障糧食安全、經(jīng)濟(jì)發(fā)展及緩解能源危機(jī)等方面起重要作用。因而，玉米籽粒產(chǎn)量形成的生物學(xué)基礎(chǔ)解析吸引了許多科學(xué)家的關(guān)注，成為遺傳學(xué)、發(fā)育生物學(xué)和作物育種學(xué)等學(xué)科的重大科學(xué)問(wèn)題。隨著群體遺傳學(xué)、基因組學(xué)、發(fā)育生物學(xué)和分子生物學(xué)等學(xué)科的理論和技術(shù)發(fā)展及其在玉米研究中的應(yīng)用，玉米籽粒產(chǎn)量及其相關(guān)性狀形成的生物學(xué)基礎(chǔ)等研究領(lǐng)域取得了重要進(jìn)展。由于玉米單穗籽粒產(chǎn)量由穗粒數(shù)和粒重兩個(gè)因子組成，本文將主要圍繞穗粒數(shù)和粒重發(fā)育相關(guān)基因及其調(diào)控網(wǎng)絡(luò)，簡(jiǎn)要介紹國(guó)內(nèi)外在這一領(lǐng)域所取得的主要成果。

1 穗粒數(shù)與雌花序發(fā)育

玉米果穗是雌花序上各類分生組織按其固有模式分化和發(fā)育的最終結(jié)果?；ㄐ蚍稚M織（inflorescence meristem，IM）產(chǎn)生數(shù)目不等的成對(duì)小穗分生組織（spikelet-paired meristem，SPM），而每個(gè)SPM進(jìn)一步分化出2個(gè)小穗分生組織（spikelet meristem，SM），隨著小花分生組織（floral meristem，F(xiàn)M）的產(chǎn)生，花序分化終止，這一過(guò)程稱之為花序發(fā)育；FM經(jīng)花器官分化和發(fā)育形成小花，這一過(guò)程稱之為小花發(fā)育[1]。授粉后，小花經(jīng)胚和胚乳發(fā)育形成籽粒。由此可見(jiàn)，花序和小花中各類分生組織的正常起始和發(fā)育與花序上最終形成的小花數(shù)目和每穗籽粒數(shù)密切相關(guān)。由于花序建成和小花發(fā)育是籽粒產(chǎn)量的生物學(xué)基礎(chǔ)，因而，這一研究領(lǐng)域吸引了許多科學(xué)家的關(guān)注。目前，對(duì)玉米花序建成和小花發(fā)育調(diào)控的認(rèn)知主要來(lái)自于對(duì)突變體的深入分析。已鑒定的控制花序上各類分生組織分化和花器官發(fā)育的基因分別參與了以下幾條調(diào)控途徑。

1.1 CLAVATA-WUSCHEL（CLV-WUS）負(fù)反饋調(diào)控途徑

參與該途徑的基因，通過(guò)調(diào)控分生組織中干細(xì)胞分裂和分化的平衡，維系干細(xì)胞數(shù)目并源源不斷產(chǎn)生新的組織或器官[2-3]。玉米中參與該途徑的基因包含：分別編碼擬南芥CLAVATA1（CLV1）、CLV2和CLV3同源蛋白的基因（）[4]、（）[5]和[6]，編碼CLV3/EMBRYO-SURROUNDING REGION（CLE）類信號(hào)肽分子的基因（）、和[6-7]，以及編碼下游效應(yīng)分子的基因（）[8]和Z（）等[9]。這一途徑中各基因間的相互關(guān)系已有許多綜述，不再贅述，僅以圖1作簡(jiǎn)單描述（圖1）。與擬南芥中形成受體復(fù)合體不同，玉米TD1和FEA2可能在不同的遺傳途徑發(fā)揮作用。

近年來(lái)研究證實(shí)，編碼SQUAMOSA promoter binding protein（SBP）轉(zhuǎn)錄因子的（）和也參與花序分生組織活性的調(diào)控。和主要在SPM的外緣表達(dá)，或單突變體的花序無(wú)明顯異常表型，而雙突變體的雌花序分化提前終止、頂部異常膨大、穗行數(shù)增加、果穗變短，顯示出這兩個(gè)基因功能的部分冗余[10]。過(guò)表達(dá)或的植株其花序分化也受到抑制并提前終止、花序變短、穗粒數(shù)減少。同時(shí)，也是GIF1（GROWTH-REGULATING FACTOR（GRF）-INTERACTING FACTOR 1）的靶基因，其表達(dá)受GIF1調(diào)控。功能喪失突變體也表現(xiàn)出與雙突變體相似的花序膨大表型[11]。其次，UB3還可結(jié)合到（）和（）啟動(dòng)子，調(diào)控和的表達(dá)，進(jìn)而參與細(xì)胞分裂素（CKs）合成和信號(hào)途徑[12]。另外，也可通過(guò)調(diào)控和參與到CLV-WUS途徑來(lái)調(diào)節(jié)花序分生組織的大小和小穗原基的起始，從而調(diào)控穗行數(shù)[12]。這些研究描繪了一條以為中心調(diào)控花序發(fā)育的新途徑，即正調(diào)控，而負(fù)調(diào)控，通過(guò)連接CLV-WUS途徑（圖1）。

盡管玉米CLV-WUS途徑中關(guān)鍵基因的強(qiáng)突變導(dǎo)致雌穗頂端扁平、穗行數(shù)增加、穗長(zhǎng)變短、單穗籽粒產(chǎn)量下降，但是，和弱等位突變能維持分生組織正常發(fā)育，并通過(guò)增加IM大小和SPM原基起始數(shù)目來(lái)增加穗行數(shù)，最終導(dǎo)致穗粒數(shù)增加，提高了單穗籽粒產(chǎn)量[6,8]。而在自交系群體中，編碼區(qū)的一個(gè)A/G變異引起第220位的絲氨酸變?yōu)樘於０罚撟儺愇稽c(diǎn)與穗行數(shù)關(guān)聯(lián)[10]。另外，在下游約60 kb位置，有一個(gè)主效QTL。為一段非編碼DNA，其中一個(gè)轉(zhuǎn)座子片段的插入/缺失可調(diào)節(jié)的表達(dá)水平，進(jìn)而導(dǎo)致穗行數(shù)的數(shù)量變異[13]。這些研究說(shuō)明，玉米花序發(fā)育關(guān)鍵基因的弱突變可以引起籽粒產(chǎn)量相關(guān)性狀的數(shù)量變異，基因組上非編碼區(qū)的變異也可通過(guò)調(diào)節(jié)花序發(fā)育關(guān)鍵基因的表達(dá)水平，進(jìn)而引起籽粒產(chǎn)量相關(guān)性狀的數(shù)量變異。

1.2 激素及其信號(hào)途徑

植物激素及其信號(hào)也參與雌花序上各類分生組織的確定性和活性的調(diào)控。這些基因基于其作用途徑大致分為：1）生長(zhǎng)素合成及其信號(hào)相關(guān)基因。這些基因包括生長(zhǎng)素合成相關(guān)基因（）和（）（圖2-a）、生長(zhǎng)素運(yùn)輸和定位相關(guān)基因（）、生長(zhǎng)素信號(hào)相關(guān)基因、和（圖2-b）編碼色氨酸氨基轉(zhuǎn)移酶，催化色氨酸向吲哚-3-丙酮酸的轉(zhuǎn)變[14]；編碼一個(gè)單子葉植物特有的黃素單加氧酶[15]。和突變體均表現(xiàn)為雌雄花序上IM分化活性下降、各類次生分生組織分化受到抑制、花序分化提前終止、小花數(shù)目明顯減少[14]。編碼一個(gè)與擬南芥PINOID同源的絲氨酸/蘇氨酸蛋白激酶，可與PIN-FORMED1a（ZmPIN1a）和一個(gè)bHLH轉(zhuǎn)錄因子BARREN STALK1（BA1）互作[16-17]，參與生長(zhǎng)素極性運(yùn)輸。突變體雌雄穗分枝難以分化，小穗分生組織減少[18]。可見(jiàn)，主要參與IM分化和SPM活性維持。另外，和均編碼生長(zhǎng)素信號(hào)途徑的AUX/IAA蛋白，其突變體表現(xiàn)為與相似的表型，雌雄穗分枝數(shù)和小花數(shù)均受到嚴(yán)重抑制[19-20]。而突變體無(wú)雌穗、且雄穗無(wú)分支和小穗，表明在營(yíng)養(yǎng)和生殖發(fā)育中調(diào)節(jié)次生分生組織的起始；的這些功能受BIF1、BIF2和BIF4的調(diào)控[20-21]。除此之外，編碼一個(gè)bZIP轉(zhuǎn)錄因子，通過(guò)調(diào)控生長(zhǎng)素響應(yīng)因子（ARF）參與生長(zhǎng)素信號(hào)途徑、進(jìn)而調(diào)控雌花序SPM的確定性[22]。而（）編碼的谷氧還蛋白（GRX）能與FEA4互作，形成MSCA1-FEA4-ARF的生長(zhǎng)素信號(hào)調(diào)控途徑[23]。因此，在玉米中可通過(guò)影響生長(zhǎng)素合成、運(yùn)輸及信號(hào)相關(guān)基因，調(diào)控花序發(fā)育，進(jìn)而影響籽粒產(chǎn)量。2）激素交互作用的關(guān)鍵基因。（）編碼一個(gè)CKs誘導(dǎo)的類型A響應(yīng)調(diào)節(jié)子，在擬南芥中可正調(diào)控生長(zhǎng)素信號(hào)、負(fù)調(diào)控細(xì)胞分裂素信號(hào)[24]。在玉米突變體中，生長(zhǎng)素水平和的表達(dá)均降低，導(dǎo)致莖頂端分生組織（shoot apical meristem，SAM）膨大，葉原基起始推遲，說(shuō)明在玉米SAM中也是生長(zhǎng)素水平和運(yùn)輸?shù)恼{(diào)控因子，揭示了組織和器官發(fā)生過(guò)程中植物激素平衡調(diào)節(jié)的重要性[25]。是水稻重要株型和產(chǎn)量基因（）的同源基因[26-27]。在水稻中，IPA1既可與赤霉素（GAs）抑制因子DELLA蛋白互作干擾DELLA蛋白的降解，抑制赤霉素信號(hào)轉(zhuǎn)導(dǎo)[28]，又與獨(dú)腳金內(nèi)酯（SL）信號(hào)通路中的關(guān)鍵負(fù)調(diào)控因子Dwarf 53（D53）蛋白直接互作抑制的轉(zhuǎn)錄激活活性；IPA1還能直接結(jié)合的啟動(dòng)子并激活的表達(dá)，形成負(fù)反饋調(diào)節(jié)[29]。然而，/在水稻中的這一負(fù)反饋調(diào)節(jié)途徑在玉米中是否存在還有待進(jìn)一步研究。不過(guò)，玉米在水稻表達(dá)中則參與了CKs的合成和信號(hào)途徑，進(jìn)而調(diào)控分支分生組織的起始[12]，由此可見(jiàn)，參與多種激素信號(hào)途徑，可能是一個(gè)連接激素信號(hào)和CLV-WUS途徑的關(guān)鍵因子。隨著測(cè)序技術(shù)的發(fā)展，基于轉(zhuǎn)錄組學(xué)分析揭示了CKs和GAs在玉米花序發(fā)育中的作用及其調(diào)控關(guān)系，發(fā)現(xiàn)（）和（）可能參與GA合成和信號(hào)途徑：即RA1結(jié)合（）正調(diào)控表達(dá)，也負(fù)調(diào)控GA信號(hào)抑制子（），時(shí)空特異性地激活GA合成和代謝相關(guān)基因進(jìn)而調(diào)控GA水平，而KN1和SPY則能正調(diào)控CKs[30]（圖2-c）。這些結(jié)果說(shuō)明了花序建成和發(fā)育中激素作用的重要性和復(fù)雜性。

a：SPI1和VT2調(diào)控色氨酸依賴的生長(zhǎng)素合成。b：生長(zhǎng)素轉(zhuǎn)運(yùn)與信號(hào)相關(guān)基因及其調(diào)控途徑。c：UB3介導(dǎo)的激素交互作用。表示正調(diào)控。表示負(fù)調(diào)控

2 穗粒數(shù)與小花發(fā)育

在發(fā)育生物學(xué)上，玉米穗粒數(shù)是穗行數(shù)與行粒數(shù)的集合。它們的形成需經(jīng)歷花序形態(tài)建成和小花發(fā)育2個(gè)過(guò)程，前者決定花序上所分化的小花數(shù)目，后者決定小花育性和授粉結(jié)實(shí)潛力。而小花分生組織分化產(chǎn)生的花器官分生組織及其有序性地發(fā)育是小花發(fā)育的主要生物學(xué)事件，因此，花器官分生組織的起始和發(fā)育也與穗粒數(shù)密切相關(guān)。玉米雌、雄小花分生組織均能分化出1個(gè)外稃、1個(gè)內(nèi)稃、2個(gè)漿片、3個(gè)雄蕊和3個(gè)心皮原基，其中，內(nèi)外稃等同于雙子葉植物花的萼片，漿片等同于花瓣，說(shuō)明玉米花器官發(fā)育也遵循“ABCDE”模型[31]。盡管每朵玉米小花均能分化出兩性花所具有的花器官原基，但成熟的玉米小花仍發(fā)育成為單性花，即雄花中心皮發(fā)育被抑制、而雌花中雄蕊發(fā)育被抑制[32]，形成了同一小花中雌蕊或雄蕊選擇性發(fā)育的特征。這一特征也是玉米與其他禾谷類作物及模式植物擬南芥在小花發(fā)育調(diào)控上的區(qū)別，使得玉米小花成為花器官發(fā)育研究的理想材料。

迄今為止，在玉米中所鑒定到的花器官發(fā)育相關(guān)基因，主要包含1個(gè)A類基因Zea APETALA Homolog1（ZAP1）[33]，4個(gè)B類基因SILKY1（SI1）[31]、Zea mays MADS16 （ZMM16）/STERILE TASSEL SILKY EAR1（STS1）[34]、ZMM18和ZMM29[35]，3個(gè)C類基因Zea AGAMOUS1（ZAG1）[36]、ZMM2[37]和ZMM23[38]，3個(gè)D類基因ZAG2[36]、ZMM1[38]和ZMM25[38]，以及4個(gè)E類基因ZAG3/-（）[40]、ZAG5[41]、ZMM8和ZMM14[42-44]（圖3-a），其中，僅有SI1、ZMM16和BDE的功能解析最清楚。SI1在雄蕊和漿片中特異表達(dá)，其突變后導(dǎo)致雄蕊轉(zhuǎn)換為心皮、漿片轉(zhuǎn)換為類似于內(nèi)外稃的結(jié)構(gòu)，因而，si1突變體表現(xiàn)為雄性不育[31]。ZMM16與擬南芥B類基因APETALA3/ DEFICIENS同源，在雄蕊原基、雄蕊和漿片中特異表達(dá)。在zmm16自然突變體中，雄花漿片和雄蕊轉(zhuǎn)變成內(nèi)外稃、雌花中本應(yīng)退化的雄蕊轉(zhuǎn)變成心皮，雌、雄小花均不育[34]。BDE在小花分生組織、漿片、心皮原基和內(nèi)稃中均有表達(dá)，在內(nèi)珠被和胚珠原基表達(dá)水平最高。BDE蛋白可與ZAG1互作調(diào)控小花分生組織的產(chǎn)生和花器官分生組織的起始與活性維持。在bde突變體中，雄花產(chǎn)生額外的花器官、雄蕊發(fā)育受到部分抑制、而雌蕊發(fā)育異常激活而形成花絲，雌花產(chǎn)生內(nèi)外稃的結(jié)構(gòu)、一個(gè)胚珠上生長(zhǎng)出多個(gè)花絲[40]。這些“ABCDE”模型中的同源基因，由于直接調(diào)節(jié)花器官的發(fā)育而影響小花的育性，因此也影響授粉后果穗上的籽粒數(shù)。

除“ABCDE”花器官發(fā)育模型相關(guān)基因外，對(duì)玉米雌、雄性器官選擇性發(fā)育的調(diào)控研究，豐富了對(duì)植物小花性別決定的認(rèn)識(shí)。控制分生組織確定性的基因在性別決定中扮演重要角色。（）（）編碼APETALA2（AP2）/ERF轉(zhuǎn)錄因子，突變體的小穗分生組織確定性喪失，產(chǎn)生額外小花，并且雄花序部分小花因心皮發(fā)育產(chǎn)生花絲[45]，與其功能相似的同源基因（）則具有積加效應(yīng)[46]。而編碼的miR172靶向和，負(fù)調(diào)控它們的表達(dá)[47]（圖3-b）。另外，研究發(fā)現(xiàn)茉莉酸（JAs）和油菜素內(nèi)酯（BRs）可通過(guò)調(diào)控小花的性別進(jìn)而調(diào)節(jié)小花育性和授粉潛力。目前，玉米中已克隆了6個(gè)JAs合成和代謝相關(guān)基因，其中，編碼一個(gè)脂氧化酶[48]、編碼一種單子葉植物所特有的短鏈乙醇脫氫酶[49]和是2個(gè)同源基因，均編碼12-氧-植物二烯酸還原酶（12-oxo-phytodienoic acid reductase）[50]，這4個(gè)基因共同參與JA的生物合成。單突變體、和雙突變體均影響JA生物合成，導(dǎo)致JA水平下降，雄穗上部分小花產(chǎn)生花絲[47-49]。顯性突變體的雄花序上也發(fā)育出雌性小花、產(chǎn)生花絲。編碼一個(gè)ZmCYP94B1蛋白，參與JA代謝，即負(fù)調(diào)控JA水平[51]（圖3-b）。由此可見(jiàn)，高水平的JA是玉米雄花中雌蕊退化或者抑制心皮發(fā)育所必要的。那么，玉米雌花中控制雄蕊退化或者保持雌蕊發(fā)育的關(guān)鍵基因是什么？編碼一個(gè)尿苷二磷酸糖基轉(zhuǎn)移酶，該酶可阻斷JA生物合成；在突變體中，其雄穗發(fā)育正常、但雌穗花絲發(fā)育受到抑制[52]。雙突變體雌穗花絲恢復(fù)，而雄穗大多數(shù)小花也能發(fā)育雄蕊[53]；而雙突變體的雌穗無(wú)花絲，雄穗產(chǎn)生少量花絲[51]。結(jié)果表明，是雌花中雌蕊發(fā)育所必需的，并且阻斷JA合成有利于雌蕊發(fā)育。除了JA外，BR也在玉米小花性別決定中起著重要作用。例如，（）是一個(gè)BR生物合成途徑的酶編碼基因，在花藥發(fā)育整個(gè)過(guò)程中均有表達(dá)、也在心皮原基表層細(xì)胞中表達(dá)直至其退化；突變體的雄穗部分小花花藥退化而花絲發(fā)育，并有類似內(nèi)外稃的變形葉，成熟植株的雄穗上著生有種子，突變體的雌穗和雌花發(fā)育正常[54]。（）也參與BR生物合成途徑，其突變體表現(xiàn)為與相似的表型[55]。這說(shuō)明BR在雄蕊和雌蕊發(fā)育中起著不同作用，即BR促進(jìn)雄蕊發(fā)育而抑制心皮分生組織的分化，而調(diào)節(jié)BR在玉米雌花和雄花發(fā)育中不同功能的機(jī)理至今未知。

近年來(lái)，沉默乙烯合成途徑的（），能增加轉(zhuǎn)基因玉米家系在缺水和低氮條件下的產(chǎn)量[56]；過(guò)表達(dá)乙烯信號(hào)途徑的組分AUXIN-REGULATED GENE INVOLVED IN ORGAN SIZE（ARGOS）可增加轉(zhuǎn)基因家系和雜交種在正常和干旱條件下的穗長(zhǎng)、穗粒數(shù)及籽粒產(chǎn)量[57]。結(jié)果表明，乙烯水平和信號(hào)或直接參與花序和小花發(fā)育、或通過(guò)參與玉米對(duì)脅迫的響應(yīng)間接地影響花序和小花發(fā)育。這些發(fā)現(xiàn)也指出一條“通過(guò)調(diào)控乙烯合成和信號(hào)進(jìn)而提高玉米抗性和籽粒產(chǎn)量”的新途徑。

a：玉米花器官發(fā)育“ABCDE”模型調(diào)控基因。不同色塊代表不同類型的花器官調(diào)控基因，下方標(biāo)注代表不同花器官及其對(duì)應(yīng)輪數(shù)。A類基因決定第一輪內(nèi)稃和外稃的形成，第二輪和第三輪漿片和雄蕊的形成分別由A+B和B+C基因調(diào)控，第四輪心皮發(fā)育則由C類基因單獨(dú)調(diào)控。D類基因主要在胚珠發(fā)育中起作用，E類基因則參與所有的花器官發(fā)育調(diào)控。b：小花性別決定基因調(diào)控網(wǎng)絡(luò)。表示正調(diào)控。表示負(fù)調(diào)控

3 胚和胚乳發(fā)育

玉米籽粒由來(lái)自母本的種皮、經(jīng)雙受精產(chǎn)生的二倍體胚和三倍體胚乳3種組織組成[58]，其中，胚和胚乳分別占成熟籽粒重量的8%—10%和80%—85%，可見(jiàn)，胚和胚乳發(fā)育直接影響籽粒大小和粒重。

為研究胚和胚乳發(fā)育的遺傳調(diào)控，科學(xué)家鑒定到了許多胚和胚乳發(fā)育突變體，并將這些突變體命名為（）[59-60]或（）[61-62]或（）[63]。其中，突變體是中極端表型類型，其胚和胚乳發(fā)育嚴(yán)重遲滯，成熟突變籽粒被正常籽粒擠壓成紙片狀[63]。另外，與不同，（）突變體影響胚形態(tài)建成，導(dǎo)致籽粒不能正常萌發(fā)，胚乳可正常發(fā)育但籽粒變小[64-65]。近年來(lái)，一批突變體基因的鑒定與分離，從而對(duì)玉米胚和胚乳發(fā)育的遺傳基礎(chǔ)有了一個(gè)較為系統(tǒng)的認(rèn)識(shí)。

3.1 線粒體基因轉(zhuǎn)錄本的加工和編輯與胚和胚乳發(fā)育

在已克隆的籽粒發(fā)育突變體中，大多數(shù)基因編碼PPR蛋白家族成員。已克隆的6個(gè)基因編碼線粒體靶向的PPR蛋白，分別參與線粒體基因內(nèi)含子剪切（[66]、[67]、[68]）或RNA編輯（[69]、[70]和[71]）。同樣，已克隆的12個(gè)突變體基因中，10個(gè)編碼線粒體靶向的PPR蛋白，分別參與內(nèi)含子剪切（[72][73][74][75]和[76]）、RNA編輯（[77]、[78]、[79]和[80]）和線粒體轉(zhuǎn)錄本的表達(dá)調(diào)控（[81]）。此外，也編碼1個(gè)PPR蛋白，其功能為線粒體轉(zhuǎn)錄后的編輯[59]。這些突變體的線粒體電子傳遞鏈復(fù)合體不能正常組裝，導(dǎo)致電子傳遞、ATP合成受阻，因而，這些基因突變后會(huì)強(qiáng)烈影響胚乳細(xì)胞發(fā)育這個(gè)十分耗能的進(jìn)程[82]，同時(shí)也說(shuō)明玉米胚和胚乳發(fā)育依賴于PPR蛋白靶向線粒體基因的轉(zhuǎn)錄后加工。

3.2 質(zhì)體基因的轉(zhuǎn)錄和翻譯與胚發(fā)育

在擬南芥中，30%的胚發(fā)育突變體由質(zhì)體靶向蛋白的功能異常所引起[83]，在一定程度上說(shuō)明質(zhì)體在胚形態(tài)建成過(guò)程中扮演舉足輕重的角色。在玉米中，影響胚發(fā)育的也編碼質(zhì)體靶向蛋白，并通過(guò)不同的途徑影響胚發(fā)育。如編碼一個(gè)PPR蛋白，PPR8522可能通過(guò)與靶向質(zhì)體的σ因子（SIG6）互作，影響依賴于質(zhì)體編碼的RNA polymerase進(jìn)行轉(zhuǎn)錄的基因表達(dá)，進(jìn)而影響類囊體結(jié)構(gòu)導(dǎo)致胚致死[84]。編碼質(zhì)體起始因子IF3，影響質(zhì)體蛋白的合成[65]。編碼一個(gè)GTP酶，功能缺失后降低16S rRNA和質(zhì)體核糖體基因的表達(dá)，影響核糖體組裝，最終影響質(zhì)體蛋白翻譯[85]。編碼DNA/RNA結(jié)合蛋白WHIRLY1（WHY1），該蛋白在穩(wěn)定質(zhì)體基因組及核糖體形成過(guò)程中起著重要作用[86]。另外，編碼一個(gè)質(zhì)體核糖體蛋白PRPS9（plastid 30S ribosomal protein S9），與一樣，其功能缺失只影響胚的發(fā)育[87]。結(jié)果表明，質(zhì)體也在維持玉米胚發(fā)育過(guò)程中起著必不可少的作用。

3.4 籽粒發(fā)育與細(xì)胞核RNA轉(zhuǎn)錄和加工

近年來(lái)，從所分離的幾個(gè)突變體基因中了解玉米籽粒發(fā)育遺傳調(diào)控的新途徑。如（）編碼一個(gè)PLATZ（plant AT-rich sequence and zinc binding）家族蛋白，該蛋白可與RNA聚合酶Ⅲ的2個(gè)亞基結(jié)合，調(diào)控tRNA和5S rRNA轉(zhuǎn)錄。由于只在淀粉胚乳細(xì)胞中表達(dá)，其突變后特異影響胚乳發(fā)育[88]。編碼一個(gè)RNA外切酶，通過(guò)影響U6 snRNA 3′-末端的加工，導(dǎo)致前體mRNAs剪切異常，最終影響籽粒和植株發(fā)育[89]。編碼RRM_RBM48型RNA結(jié)合蛋白，與其他剪接體組分相互作用參與前體mRNA剪接調(diào)節(jié)，它的突變顯著改變表達(dá)基因的選擇性剪接，使得U12型內(nèi)含子被保留于轉(zhuǎn)錄本中，表現(xiàn)出小粒和幼苗致死表型[90]。而Urb2作用于前體rRNA加工，在突變體中，前體rRNA中間產(chǎn)物顯著富集，很多核糖體相關(guān)基因的表達(dá)水平也受到影響，籽粒發(fā)育和植株生長(zhǎng)都受到抑制[87]。結(jié)果表明，這些基因直接參與到了細(xì)胞核內(nèi)mRNA或者rRNA加工這一基礎(chǔ)生物學(xué)過(guò)程，因此，細(xì)胞核RNA轉(zhuǎn)錄加工對(duì)籽粒發(fā)育有著深遠(yuǎn)影響[91]。此外，則編碼SISTER CHROMATID COHESION PROTEIN 4（SCC4）的同系物，突變可破壞有絲分裂細(xì)胞周期和核內(nèi)復(fù)制，導(dǎo)致胚乳和胚胎致死[92]。這項(xiàng)新的發(fā)現(xiàn)揭示了玉米有絲分裂染色體分離和內(nèi)核發(fā)育的異常，也可導(dǎo)致籽粒發(fā)育缺陷。由于上述基因參與許多生物學(xué)過(guò)程的調(diào)控，這些基因突變常會(huì)影響包含籽粒發(fā)育在內(nèi)的、廣泛的生物學(xué)性狀，顯示出基因功能的多效性。

4 展望

基于突變體的遺傳分析，科學(xué)家已鑒定并分離了一批玉米花序、小花和籽粒發(fā)育相關(guān)基因，對(duì)許多基因的作用機(jī)理和調(diào)控途徑有了深入研究，但相較于模式植物擬南芥和模式作物水稻，玉米中所克隆的基因數(shù)目相對(duì)較少，而直接控制穗粒數(shù)和粒重的基因數(shù)目更少。為深入解析玉米產(chǎn)量及產(chǎn)量相關(guān)性狀形成的生物學(xué)基礎(chǔ)，進(jìn)一步鑒定并克隆更多新的產(chǎn)量及產(chǎn)量相關(guān)性狀的基因、闡明多基因之間的互作關(guān)系、挖掘控制產(chǎn)量相關(guān)性狀的關(guān)鍵節(jié)點(diǎn)基因并解析其調(diào)控網(wǎng)絡(luò)、探究發(fā)育相關(guān)基因的自然變異與產(chǎn)量及產(chǎn)量相關(guān)性狀的關(guān)系等，將是今后一定時(shí)期內(nèi)玉米遺傳學(xué)研究的重點(diǎn)和熱點(diǎn)領(lǐng)域。玉米籽粒著生于雌穗，雌穗上所形成的籽粒其實(shí)質(zhì)是花序和小花中各類分生組織起始、分化和發(fā)育以及授粉后的籽粒發(fā)育等生物學(xué)過(guò)程的最終結(jié)果。經(jīng)長(zhǎng)期研究已鑒定到了一批花序和小花發(fā)育相關(guān)的基因，特別是鑒定到了許多參與CLV-WUS負(fù)反饋途徑、“ABCDE”模型及激素合成和信號(hào)途徑等的關(guān)鍵基因，并對(duì)這些基因在玉米花序和小花發(fā)育中的生物學(xué)功能和作用機(jī)理與其在擬南芥、水稻中的保守性和差異性進(jìn)行了分析。但是，各類分生組織起始、分化和終止的內(nèi)外信號(hào)、CLV-WUS途徑調(diào)控干細(xì)胞增殖和分化的上下游基因及其精細(xì)調(diào)控網(wǎng)絡(luò)、小花性別分化的遺傳控制、激素及其交互作用調(diào)控花器官特別是雄蕊和心皮分化和發(fā)育的分子途徑等研究尚淺，將是玉米發(fā)育生物學(xué)重點(diǎn)研究領(lǐng)域。在籽粒發(fā)育這一研究領(lǐng)域，將進(jìn)一步鑒定胚和胚乳發(fā)育新基因和新調(diào)控途徑，重點(diǎn)發(fā)掘發(fā)育相關(guān)基因與粒重的關(guān)聯(lián)，揭示其自然變異，為粒重遺傳改良提供基因資源。另外，穗粒數(shù)、粒型和粒重等也是玉米長(zhǎng)期改良的目標(biāo)性狀，探索控制這些性狀的有利等位基因的產(chǎn)生、在育種過(guò)程中的選擇及其演化規(guī)律，也是今后重要的研究課題，并將為玉米育種提供理論指導(dǎo)和重要的遺傳資源。

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Molecular Basis of Kernel Development and Kernel Number in Maize (L.)

ZHAO Ran, CAI Manjun, DU Yanfang, ZHANG Zuxin

(National Key Laboratory of Crop Genetic Improvement, Huazhong Agricultural University, Wuhan 430070)

Grain yield per ear of maize (L.) is composed of both kernel number and grain weight. The number of kernels on an ear is determined by not only the number of kernel rows which is closely related to the inflorescence development, but also the number of fertile florets generated by the flower meristem. Therefore, those genes for inflorescence architecture and flower development are potentially involved in the genetic control of kernel number. Maize kernel is a single-seeded fruit comprised of the maternally derived pericarp, and embryo and endosperm derived from double fertilization. Both embryo and endosperm account for the vast majority of the mature kernel mass, and directly determine the kernel size and weight. In this paper, we outlined the genetic controls of kernel number with the emphasis on the inflorescence and floret related genes that are involved in the CLAVATA- WUSCHEL (CLV-WUS) feedback loop, hormone biosynthesis and signaling, floral organ development and sex determination. In particular, we described the regulatory network models for interplays among phytohormones including auxin, gibberellin, cytokinin and strigolactone in the inflorescence architecture and floral organ development. We also summarized those embryo and endosperm developmental genes involving in processing and editing of mitochondrial transcripts, transcription and translation of some chloroplast DNAs as well as nuclear RNAs. Most of these genes encode PPR proteins targeted to mitochondria or plastids. Recently, several studies have identified a new pathway to control kernel development by regulating the transcription and processing of pre-mRNA within the nucleus. Here, we also discussed the association between these genes and kernel number or kernel weight, and the potential areas of research for deciphering molecular mechanisms of grain yield in maize.

L.; kernel number per ear; kernel weight; inflorescence; floret; embryo; endosperm

10.3864/j.issn.0578-1752.2019.20.001