激素调控植物成花机理研究进展

邹礼平，潘铖，王梦馨，崔林，韩宝瑜

综 述

激素调控植物成花机理研究进展

邹礼平，潘铖，王梦馨，崔林，韩宝瑜

中国计量大学，浙江省生物计量及检验检疫技术重点实验室，杭州 310018

开花是植物对环境的适应性表现，是在多种外源和内源信号形成的复杂成花调控网络下完成。植物激素作为最重要的内源信号参与者，在成花进程中扮演着重要角色。近年来，光周期等成花途径和表观遗传调控中激素的作用机理不断被解析。研究发现激素间存在协同和拮抗作用，并证实多种激素参与赤霉素(gibberellins, GA)途径中DELLA蛋白介导的多种成花调控途径。本文主要综述了GA在植物成花中的调控机理，同时探讨了脱落酸(abscisic acid, ABA)、生长素(auxin, IAA)、细胞分裂素(cytokinin, CTK)、水杨酸(salicylic acid, SA)、茉莉酸(jasmonic acid, JA)和乙烯(ethylene, ET)等其他内源激素在成花中的作用及其与DELLA、miRNAs和转录因子(transcription factor, TFs)等通路串联调控，为全面解析激素调控植物成花的网络提供参考。

植物激素；花芽分化；成花调控；信号传导

开花是植物对环境的适应性表现，是植物从营养生长向生殖发育的转变，是决定植物繁殖成功与否的重要环节，本质是茎顶端分生组织(shoot apical meristem, SAM)由营养生长时期分化产生叶片转变为生殖发育时期形成花、果实和种子的过程[1]。植物成花过程可分为花的诱导、花芽分化和花器官的发育3个阶段，此过程与开花时间、开花数量、开花质量和花期长短密切相关，同时还对植物的观赏、食用和药用的经济价值产生直接影响[2]。成花过程是一个复杂的生理过程，该过程受外部和内部因素的共同调控，如光周期、温度以及内源激素介导的多种途径调控[2~4]。在过去几十年，通过对拟南芥()的成花生理和分子机制的研究，发现光周期途径、春化途径和环境温度途径主要传递光和温度等外部信号；而自主途径、赤霉素途径和年龄途径在很大程度上以内源信号为主[1,2,5~7]。可见，在自然状态下植物成花是对多种环境和内源信号识别和整合后作出的应答。

植物内源激素(plant endogenous hormones)参与植物的整个生命过程，通过在植物体内构建复杂完整的信号网络，传递外源或内源信号来调控植物的生长发育。因此，激素信号对于成花的影响非常重要[8,9]。在特定的条件下，激素信号的调控往往是将不同激素信号汇集后通过改变关键成花基因的表达水平来实现[10]。赤霉素(gibberllins, GA)作为赤霉素途径中主要的信号因子，在成花过程必然发挥着关键性的作用，但其他激素如脱落酸(abscisic acid, ABA)、生长素(auxin, IAA)、细胞分裂素(cytokinin, CTK)、水杨酸(salicylic acid, SA)、茉莉酸(jasmonic acid, JA)和乙烯(ethylene, ET)等，也是参与激素调控网络不可缺少的部分[3,11]。对于温室种植或精细化管理的作物而言，通过光周期和温度等控制外部信号可实现对成花的调控；但是对于大田种植的作物而言，则存在易被干扰、成本较高和可操作性差等缺点。因此，研究成花过程中激素的调控作用，解析植物体内信号调控网络，可为大田作物生产提供指导借鉴。本文主要对激素调控植物成花的机理研究进行了综述，并总结出部分激素互作通路模式图(图1)，以期为更好地研究植物花的诱导、花芽分化和花器官发育中激素作用机理和调控机制提供参考。

1 赤霉素途径

GA是一类四环二萜类化合物，在植物生长发育过程中起着重要的调节作用。迄今为此，自然界中发现的GA形态结构超过136种，但是只有GA1、GA3、GA4和GA7少数形态具有生理活性[12]。近年来，随着分子遗传学和功能基因组学的不断发展，GA调控植物生长发育的模式被解析的十分透彻[13,14]。越来越多的研究表明，GA在去抑制和信号转导等方面发挥着重要的作用[14,15]。GA信号转导主要借助于GID1 (GA insensitive dwarf 1)、DELLA蛋白和介导DELLA蛋白降解的其他调控因子实现，可见DELLA蛋白是GA合成及其信号转导过程中的核心因子，在GA合成以及其信号转导中发挥着重要作用。

1.1 GA与植物成花

赤霉素途径调控成花是最早被发现的4条成花途径之一，拟南芥内源GA合成受阻或者破坏GA在体内的信号转导过程，成花进程均会受到影响[16]。GA信号转导是由活性GA激活的，而GA作为可移动的分子，可通过细胞膜在细胞间进行运输[17]。细胞间GA的动态平衡主要由GA合成途径中关键限速酶基因和、失活和降解途径中氧化酶基因调控。GA信号转导依赖一类核蛋白DELLA的介导[18]，DELLA蛋白被认为是植物生长发育和成花的抑制因子。水稻(L)中仅存在一个基因编码DELLA蛋白[19,20]，而拟南芥存在5个特异性的基因，包括(GA insen­sitive)、(repressor of GAL-3)和3个gal-3-like蛋白的抑制基因(、和)，这些基因既存在功能的冗余又具有特异性[8,21]。拟南芥突变体在短日照下不开花，在长日照下呈现中度晚花现象[22]。该现象揭示赤霉素途径调控低于光周期调控，当光周期调控不起主导作用时，赤霉素途径的重要性被凸显出来。但是近期研究发现，无论光周期调控信号是否存在，GA都具有独特的调控模式促进成花。Porri等[23]发现长日照下GA也可以上调FT (flowering locus T)和TSF (twin sister of FT)蛋白的表达水平促进成花。Galvão等[24]发现环境温度途径诱导拟南芥成花需要借助GA信号转导，DELLA在长日照下可沉默叶片中miR172和茎尖的基因参与自主途径抑制成花[25]，DELLA也下调年龄途径中miR156的靶基因(squamosa promoter bi­nding protein-like)参与成花[22]。可见GA信号参与年龄、自主和环境温度等途径的调控[22,24,26~28]。FT蛋白的合成部位在叶片，但其被运送至SAM中才发挥作用[11]，因此GA调控成花的作用部位分为叶片和SAM。

成花途径关键基因用黄色高亮标记，红色和绿色分别代表激素的作用，红色代表促进、绿色代表抑制；虚线箭头代表迁移，→代表正调控，┤代表负调控，双向符号代表互相作用。GA：赤霉素；ABA：脱落酸；IAA：生长素；CTK：细胞分裂素；SA：水杨酸；JA：茉莉酸；ET：乙烯。CO: constans; FT: flowering locus T; AP1: apetala 1; SOC1: suppressor of overexpression of constans; LFY: leafy; SPLs: squamosa promoter binding protein-like; BOIs: botrytis susceptible1 interactors; PIFs: phytochrome interacting factor; AREB: ABA responsive element binding protein; ABI: abscisic acid-insensitive; HDA6: histone deacetylase 6; FLC: flowering locus C; SVP: short vegetative phase; MYC: myelocytomatosis proteins; JAZ: jasmonate ZIM-domain protein; MYB33: MYB domain protein 33; TFL: terminal flower。

1.2 叶片中的GA调控

众多的研究表明，当植物体内GA含量较低或者GA信号传递受阻的情况下，基因表达水平处于较低水平；而当叶面上外源喷洒GA或恢复GA信号传递时，基因表达水平上调[23,24,27~29]。这些结果支持长日照下GA可增强基因的转录活性这一观点。但也有研究发现叶面喷洒GA既不能改变野生型植株在短日照下基因的转录水平，也不能改变长日照下突变体基因的转录水平[29,30]。所以，长日照下GA是否调控基因的表达量还需要更多的研究来验证。

GA可通过多种机制调节基因的表达水平实现成花调控[23,24,27,28]。AP2 (apetala 2)类蛋白负调节叶片中基因的转录活性，而叶片中DELLA可抑制miR172的表达，实现对miR172靶基因的上调[31~33]。Yu等[27]也发现GA对miR172的调控是借助于DELLA和miR172的正调控因子SPLs来实现。当然部分(如)基因编码序列可直接与基因序列结合，并激活基因转录[34]。Yu等[27]还指出DELLA组成型激活表达后，miR172的表达量被显著下调，可能是由于DELLA与SPLs蛋白结合引起的，同时会引起基因转录水平下调。在突变体中过表达miR172可改善其晚花现象[31]，这也证明DELLA可能是通过调控模式增强对的转录抑制。

DELLA除了可激活基因的抑制因子外，还会干扰关键转录激活因子CO (constans)蛋白的功能。DELLA可与CO或含有CO结构域的类似物结合，使其与DNA互作而丧失功能[35,36]。因此，不论是GA含量降低还是增强DELLA蛋白水平，其最终结果都是导致和的转录水平降低，这与CO蛋白的稳定性恰好一致[23,30]。体外研究发现，DELLA可阻止CO和NFYB(nuclear transcription factor Y subunit B)互相结合，从而使CO失去激活的功能[35,37]。CO与NFY (nuclear transcription factor Y)复合物的主要功能是维持染色体上位点的特异性结构，从而有利于的转录激活[38]。因此，DELLA可通过降低CO蛋白功能来阻止染色体上位点的特异性结构的形成[30]。但是，Hou等[28]提出DELLA与NFYB和NFYC也可以互相结合，所以DELLA的调控机制可能更为复杂。

DELLA蛋白可与多种转录因子结合同时抑制CO蛋白功能和基因的转录激活，其本质是通过与转录因子结合互作的方式降低与DNA的结合能力[39]。如光敏色素互作因子(phytochrome interacting factor 4)是的激活因子，在温敏途径中CO蛋白也可被互作激活。DELLA与结合后，的功能被抑制[40~42]。可见，GA利用DELLA与PIF4或PIFs类转录因子的互作机制调控植物成花时间[43]。

除了结合互作的方式外，DELLA还可通过其他机制影响转录因子[39]。Li等[44]研究发现，DELLA与转录因子的结合，不但产生“隔离”的作用，还能降解。DELLA还可以引导转录抑制因子作用于特定的基因位点，如BOIs (botrytis susce­ptible1 interactors)蛋白[45]。BOIs蛋白在花芽分化期富集，但需要依赖于DELLA才能被引导至启动子区域富集并与位点结合，抑制的转录[46]。除了依赖于DELLA的方式外，BOIs蛋白也可通过其CCT结构域与CO蛋白结合，干扰CO与DNA的识别机制[46]。同样，DELLA蛋白还可与FLC (flowering locus C)形成复合物阻碍基因的转录激活[47]。

1.3 SAM中的GA调控

SAM是GA调控成花的另一个作用部位。外源喷洒GA不能激活短日照下叶片内基因的表达，但却可以促进野生型、突变体和突变体成花[23,29,48,49]。非成花条件下，叶片中高含量GA诱导SAM成花，因此Hisamatsu和King[29]提出GA成花调控途径不借助于叶片中的成花基因。这可能是叶片中合成的GA被运输至SAM才激活成花基因表达，也可能是GA拥有不依赖于叶片中FT蛋白的调控机制[17]。Zhu等[50]发现叶片中合成FT蛋白在NaKR1 (sodium potassium root defective 1)蛋白作用下被运输至SAM中发挥作用。虽然GA在植物体内的精准分布情况还缺乏研究，但是GA可在细胞间被主动运输已被广泛认可[51,52]。研究发现GA4含量会在SAM花芽分化期急剧上升，与成花进程密切相关；但是通过分子水平的研究发现，该阶段SAM中与GA4生物合成相关基因并未提前呈现上调趋势，因此GA4含量的增加是由于SAM以外的部位运输补充[17]。NFL (no flowering in short day)转录因子是短日照下GA稳态的关键调控因子，突变体的SAM中GA生物合成和分解代谢相关基因相对野生型分别呈现下调和上调的现象，这表明该突变体的SAM中GA呈现低活性状态；但在长日照条件下，突变体与野生型类似，表现为开花表型，因此NFL及其靶基因的调控与光周期调控也密切相关[53]。

SAM中GA含量变化受到多种成花基因的影响。Andrés等[54]发现长日照下SAM中GA合成关键酶基因(gibberellin 20-oxidase 2)表达量在花芽分化期显著增加，他们认为基因表达的积累与FT蛋白的激活有关，FT蛋白通过下调成花抑制因子SVP (short vegetative phase)的表达水平来增加GA20ox2的表达量。因此，在长日照下FT信号运输至SAM后，可促进GA积累，促进花芽分化。Li等[55]发现高GA含量又可反馈抑制基因表达，他们认为SVP是SAM中GA生物合成相关基因的关键调控者。FLC/SVP复合物可上调(gib­berellin 2-oxidase)的表达促进GA的降解，还可促进GA合成关键酶GA3ox (gibberellin 3-oxidase)的抑制因子(tempranillo 1)和的表达[47,54]。因此，SVP/FLC复合物可以影响GA合成和代谢相关酶来调控GA在SAM中的动态平衡。除了调控GA生物合成和分解代谢的方式外，DELLA可将GA信号传递到多种调控途径。DELLA可激活miR159的转录表达，抑制MYB33 (MYB domain protein 33)的活性，从而完成对花分生组织特异性基因(leafy)的抑制，延缓成花进程[56~59]。也有研究指出，GA信号可直接上调的激活因子(suppressor of overexpression of constans)的表达，实现对LFY的激活，该过程不依赖于DELLA和miR159/MYB33调控途径[56,60]。但是，Yu等[27]发现DELLA可抑制SPLs的转录来下调SOC1的表达水平；也有研究指出在长日照条件下，在花芽分化期SOC1可引起SAM中部分表达量的上调，从而实现自我调节的反馈回路[23,61]。可见，GA对LFY的调控存在多种复杂的调控机制。

GA也参与SAM中由miR156及其靶基因调控的年龄途径[62]。miR156-SPLs调控模式在进化上较为保守，随着植物生长发育逐渐下调miR156的水平导致SPLs的积累增加；SPLs拥有众多参与SAM成花调控的靶基因，如miR172、、(apetala 1)和(fruitful)等成花基因[62~64]。外源喷洒GA仅能轻微缓解过表达miR156植株的晚花表型[27,65]，可见在SPLs积累过少时，GA对DELLA蛋白的降解并不能激活成花。所以，GA参与年龄途径的调控发生在mi156表达量降低后，参与增加SPLs的积累调控。DELLA蛋白对的调控可分为转录和转录后两个水平。DELLA蛋白抑制茎尖不同基因的转录激活[23,24]。Park等[66]和Zhang等[67]均发现DELLA与染色质重塑因子PKL(pickle)的拮抗结合可抑制基因的转录。而转录后的调控是DELLA蛋白直接与SPLs结合，降低SPLs结合靶基因的活性[27,65]。越来越多的研究已经证实GA通过DELLA-SPLs互作机制调控成花，在短日照条件下这种互作机制尤为显著[27,65,68,69]，但GA的具体作用与的种类密切相关。在短日照下突变体与GA缺陷型突变体均呈现为极晚花表型，因此Hyun等[65]认为是DELLA在短日照下调控的关键性靶基因，只有当GA充足并消除DELLA对SPL15的抑制作用，SPL15与SOC1才能协同诱导FUL的表达，影响SAM其他成花基因的表达。但Xu等[69]的研究结果指出短日照下的成花调控作用不是唯一的，原因是序列存在高度的冗余。相反，在花分生组织中当DELLA与SPL9结合后，有助于激活AP1启动子的转录表达[70]。因此，DELLA与SPLs的互作需要根据SPL的种类及其调控的DNA序列具体分析。

2 其他激素途径

2.1 JA

JA及其衍生物属于脂质类植物激素，JA类衍生物的信号途径及应对逆境胁迫的反应机制被研究的较为透彻[71,72]，但在花期调控中的作用研究较少。拟南芥中参与JA应答的HDA6 (histone deacetylase 6)参与染色质的去乙酰化过程，抑制基因表达，这表明HDA6是JA参与成花调控的关键因子[73~75]。有研究显示，拟南芥JA合成缺陷型突变体表现为雄性不育，同时发现突变体的花丝延伸能力、花粉成熟和花药开裂程度均受到影响[76,77]。同时，双基因突变体也呈现短花瓣、短雄蕊花丝和花药不开裂等现象[78]。而外源喷洒JA后，随着JA含量增多调节花丝成熟的(auxin respo­nse factor 6)和基因在花药开裂期大量表达，可见JA可促进雄蕊和雌蕊成熟[78]。研究表明，和分别是miR167和miR160的靶基因[78,79]，因此JA与miR167和miR160共同控制和参与成花调控[80]。Zhai等[81]还发现JA可借助JAZ (jasmonate ZIM-domain protein)蛋白将信号传递给转录因子MYCs (myelocytomatosis proteins)，来抑制的表达并延迟成花。虽然以上结果显示JA参与花器官发育或抑制的表达，但其在成花途径中的作用还缺乏研究，与其他激素是否存在串联调控机制也未被证实。

2.2 ABA

ABA是一类倍半萜类植物激素，参与植物蛋白质和脂质合成、种子脱水耐受、种子休眠和成花等生长发育过程[82]，同时ABA还参与多种非生物胁迫应答[83,84]。目前，ABA信号是否参与花芽分化仍存在争议，很多报道相互对立[85,86]。生理研究发现，ABA积累被认可有利于木本植物温州蜜柑()的花芽孕育[87]；但是在温州蜜柑花芽诱导期，ABA处于较低水平，在花原基形成时才上升到较高水平，故ABA对花芽分化的作用因所处阶段而异[88]。ABA在陆地棉()[89]、苹果()[90]的花芽分化期含量逐渐增高，可见高浓度ABA有利于花芽分化；但高含量的ABA不利于龙眼()的花芽形成[91]。在草本植物中，内源ABA是打破百合花()鳞茎休眠促进花芽分化的关键物质[92]，ABA在菊花()花芽分化期呈现为逐渐升高的现象[93]。基因的研究发现，ABA可激活和基因表达，有利于拟南芥的花芽分化[94,95]。在长日照下，和突变体呈现晚花现象，而在短日照条件下表现正常[94,95]。

ABA信号可能参与激活转录或增强CO蛋白功能。ABA可磷酸化激活ABA反应元件结合蛋白(ABA responsive element binding protein, AREB)来促进的转录[96~99]。突变体中转录处于低水平并呈现晚花表型[100,101]；但在ABA缺陷型的突变体中，表达量虽然呈现下调趋势，却呈现极早花表型[100,102]。因此，ABA是否通过调控转录有待进一步研究。ABA还影响CO蛋白功能和信号传递[95]。ABA可泛素化降解ABI3 (abscisic acid-insensitive 3)，释放与ABI3结合的CO蛋白来促进成花[35,103,104]。ABA还调控MYCs转录因子抑制FT蛋白表达，GA也存在MYC3-FT调控模式，JA调控也存在类似机制，因此ABA、GA和JA存在串联调节CO、FT蛋白功能的现象[11,81,105]。ABA还可负调控下游基因延迟成花。ABA可上调bZIP转录因子ABI5 (abscisic acid-insensitive 5)和AP2结构域转录因子ABI4 (abscisic acid-insensi­tive 4)的表达来激活转录[106,107]，降低表达量，延迟拟南芥成花。而的表达可被GA上调[56,60]，可见SOC1可能是GA和ABA信号进行串联调控的关键点之一。

2.3 ET

植物催熟激素ET与果实成熟、叶片衰老、胁迫应答和成花过程都密切相关[108]。ET在植物组织内分布具有广泛性，但只有当叶片损伤、成熟或被切除才会造成ET的合成增加。有研究发现ET合成受抑制的拟南芥突变体呈现出早花表型[109]，而ET组成型表达的突变体在短日照条件下呈晚花表型，可见ET可抑制拟南芥成花。Achard等[110]认为ET可促进DELLE蛋白的积累，抑制GA信号并延迟成花。低温环境下的成花延迟现象被认为属于ET调控，Alonso等[111]认为由于ET的抑制作用，虽然春化途径后拟南芥体内促进成花的miRNA被激活，但不呈现开花现象。ET可上调甘蓝型油菜()中的表达表达量，在增强植物抗病性同时可促进的表达来延迟成花[112]。虽然ET可调控DELLA和HAD19蛋白实现对花期的调控，但ET与其他激素在成花途径中的串联作用机制还需要深入研究。

2.4 IAA

IAA是最早被鉴定的植物激素，影响植物细胞的伸长、分化，参与种子发育、侧根形成、根和叶片的生长发育等多种生理过程[19]。同时IAA也参与植物成花调控。Mai等[113]发现与IAA缺陷型突变体(auxin resistant 2)在短日照下延迟成花。外源施加不同浓度IAA溶液会影响花朵的正常发育[114]。IAA是局部合成，经过极性运输至作用部位，在植物体内呈现梯度分布，这种动态分布与成花进程密切相关[115]。PIN (pin-formed)蛋白家族与IAA的极性运输密切相关[25]，拟南芥突变体缺失IAA的极性运输能力，出现针状花序，花、维管组织发育缺陷[26]，外源喷洒IAA可以逆转这种情况诱导成花[116]。Przemeck等[117]发现突变体仅能形成裸花序柄，因此IAA响应因子ARF5 (auxin response factor 5)活性被认为与花原基的启动密切相关。与花器官发育相关基因、(aintegumenta)和(aintegumenta-like 6)均属于ARF5的靶基因[118]。ARFs和IAA还可以通过促进和的表达[119,120]、抑制DELLA蛋白表达[121]的形式参与到GA生物合成和信号传导的过程。可见，IAA可以通过调节GA含量和促进DELLA降解的方式促进成花。

2.5 CTK

CTK是一类N6-取代的嘌呤衍生物，参与细胞的增殖和分化，与植物生长发育密切相关，在开花植物中CTK具有延缓衰老的作用[122]。尽管CTK是否参与成花转变目前还存在争议，但CTK调控花分生组织细胞的分裂和分化已被证实[123]。CKX (cyto­kinin oxidase/dehydrogenase enzymes)是催化降解CTK的关键酶，双突变体呈现异常膨大的花序和花分生长组织，因此CTK参与花芽分化中细胞分化的调控[124]。Corbesier等[125]发现成花刺激后叶片和韧皮部中内源CTK含量迅速增加；在短日照下，外源施加CTK可诱导营养生长期植物在细胞层面进行成花转变[126]。可见，CTK含量增加与成花转变的存在密切联系。此外，CTK可下调的表达水平，促进AP2蛋白表达，使植物呈现花瓣增加、雄蕊和心皮增殖等缺陷型花型[31]。可见CTK与GA信号在miR172和AP2途径实现串联调控，但CTK参与成花调控的机制尚未被完全解析[127]。

2.6 SA

SA可促进成花、调节种子发芽、抑制顶端优势、促进测生生长、调节膜透性等多种植物生长发育[22]。目前，有关SA调控成花的研究报道越来越多。如4 μmol/L浓度的SA可促进烟草()愈伤组织形成花蕾[128]。苍耳属植物韧皮部的SA含量仅在开花期能检测到[129]。外源喷洒浓度为3~ 10 μmol/L的SA溶液，可刺激对光周期不敏感的柠檬属植物成花[130]。这些发现均显示出SA含量增加在诱导成花或促进花器官发育中的作用。但是外源施加SA又可缓解由营养不良胁迫引起的牵牛()的早花现象[131]，因此SA对成花的调控与植物所处状态密切相关[131,132]。外源施加SA溶液或紫外照射可诱导SA的积累，来抑制野生型拟南芥FLC转录因子的表达，从而促进成花[130]。但在SA缺陷型突变体中SA是否存在抑制转录并促进成花的机制仍有争议，这是由于和的表达在短日照和长日照条件下是不同的。在长日照条件下，SA缺乏植物的和的表达水平与野生型相比下降约50%；在短日照条件下，SA缺乏植物的表达量与野生型相比增加2~3倍，但的表达两者间无显著差异[130]。同时，外源施加SA可逆转突变株的晚花表型，但在长日照下对突变株无显著改善现象[133]。可见，SA参与成花调控网络的串联点可能位于CO下游和SOC1上游区域，但具体机制以及SA是否参与成花调控还有待进行深入研究。

3 结语与展望

植物成花调控不仅受外界环境因子影响，而且植物体内的各种激素存在互相协同和拮抗作用，是一个复杂的调控过程。植物激素调控是植物感受外部环境变化信号，利用多种激素的协同或拮抗的作用调整自身的生长和分化进程，增强对环境适应能力的调控方式。最新的研究表明，以DELLA介导的GA信号调节中枢及其调控的多种成花因子(如CO、FT、LFY和SOC1等)，在GA和其他成花途径或激素信号途径关键调控因子的互相作用中发挥着重要作用。目前，对于激素调节植物成花的机制还未被深入解析，在不同植物的成花进程和花器官发育中激素调控机制、激素的动态变化以及在不同组织或细胞的精准分布都尚待进一步阐明。随着高通量测序技术的发展以及转录组、蛋白质组和代谢组等手段在成花调控研究中的应用，必将会全面解析激素调控植物成花的网络途径。

今后对激素调控成花机理的研究可能主要集中在以下几个方面：(1)进一步阐明激素在不同环境下与各种成花途径互作的分子机制，以及多种激素在时间和空间上协同或拮抗的串联互作机制。(2)表观遗传机制及其对植物成花的生理、代谢和分子调控影响，解析激素调控成花的表观遗传规律。随着气候变化的加剧，表观遗传对成花诱导的影响越来越显著，而植物激素信号在表观遗传调控营养期到生殖期的转变过程中不可或缺。DNA甲基化、组蛋白翻译后修饰和miRNAs剪切等表观遗传调控将指导人们更好地开发适应新环境挑战的植物。(3)应用外源激素调控花芽分化或花器官发育的可行性。不同物种、品种等激素调控的差异性较大，对开花植物特别是附加值较高的花卉植物的调控可借助温室大棚调控光周期或温度等手段来实现。但是对于大田种植或附加值较低的植物，此方法成本较高。因此研究开发和应用外源激素控制成花对指导农业生产具有重要意义。

[1] Bäurle I, Dean C. The timing of developmental transi­tions in plants., 2006, 125(4): 655–664.

[2] Amasino R. Seasonal and developmental timing of flowering., 2010, 61(6): 1001–1013.

[3] Kazan K, Lyons R. The link between flowering time and stress tolerance., 2016, 67(1): 47–60.

[4] Burgarella C, Chantret N, Gay L, Prosperi JM, Bon­homme M, Tiffin P, Young ND, Ronfort J. Adaptation to climate through flowering phenology: a case study in., 2016, 25(14): 3397– 3415.

[5] Sun CH, Deng XJ, Fang J, Chu CC. An overview of flowering transition in higher plants., 2007, 29(10): 1182–1190.孙昌辉, 邓晓建, 方军, 储成才. 高等植物开花诱导研究进展. 遗传, 2007, 29(10): 1182–1190.

[6] Andrés F, Coupland G. The genetic basis of flowering responses to seasonal cues., 2012, 13(9): 627–639.

[7] Mutasa-Göttgens E, Hedden P. Gibberellin as a factor in floral regulatory networks., 2009, 60(7): 1979–1989.

[8] Santner A, Estelle M. Recent advances and emerging trends in plant hormone signalling., 2009, 459(7250): 1071–1078.

[9] Wolters H, Jürgens G. Survival of the flexible: hormonal growth control and adaptation in plant development., 2009, 10(5): 305–317.

[10] Conti L. Hormonal control of the floral transition: Can one catch them all?., 2017, 430(2): 288–301.

[11] Bao SJ, Hua CM, Shen LS, Yu H. New insights into gibberellin signaling in regulating flowering in., 2020, 62(1): 118–131.

[12] Li JY, Li CY, Smith SM. Hormone metabolism and signaling in plants. Academic Press: New York, NY, 2017: 107–160.

[13] Sun TP, Gubler F. Molecular mechanism of gibberellin signaling in plants., 2004, 55: 197–223.

[14] Gonzalez DH. Plant transcription factors. Academic Press: New York, NY, USA, 2016: 313–328.

[15] Sun TP. The molecular mechanism and evolution of the GA-GID1-DELLA signaling module in plants., 2011, 21(9): R338–R345.

[16] Wilson RN, Heckman JW, Somerville CR. Gibberellin is required for flowering inunder short days., 1992, 100(1): 403–408.

[17] Eriksson S, Böhlenius H, Moritz T, Nilsson O. GA4 is the active gibberellin in the regulation oftransc­ription andfloral initiation., 2006, 18(9): 2172–2181.

[18] Harberd NP. Botany: Relieving DELLA restraint., 2003, 299(5614): 1853–1854.

[19] Dinesh DC, Villalobos LIAC, Abel S. Structural biology of nuclear auxin action., 2016, 21(4): 302–316.

[20] Ljung K, Bhalerao RP, Sandberg G. Sites and homeo­static control of auxin biosynthesis induring vegetative growth., 2001, 28(4): 465–474.

[21] Richter R, Behringer C, Zourelidou M, Schwechheimer C. Convergence of auxin and gibberellin signaling on the regulation of the GATA transcription factorsandin., 2013, 110(32): 13192–13197.

[22] Campos-Rivero G, Osorio-Montalvo P, Sánchez-Borges R, Us-Camas R, Duarte-Aké F, De-la-Peña C. Plant hormone signaling in flowering: An epigenetic point of view., 2017, 214: 16–27.

[23] Porri A, Torti S, Romera-Branchat M, Coupland G. Spatially distinct regulatory roles for gibberellins in the promotion of flowering ofunder long photoperiods., 2012, 139(2): 2198–2209.

[24] Galvão VC, Horrer D, Küttner F, Schmid M. Spatial control of flowering by DELLA proteins in., 2012, 139(21): 4072–4082.

[25] Tanaka H, Dhonukshe P, Brewer PB,Friml J. Spatiotemporal asymmetric auxin distribution: a means to coordinate plant development., 2006, 63(23): 2738–2754.

[26] Okada K, Ueda J, Komaki MK, Bell CJ, Shimura Y. Requirement of the auxin polar transport system in early stages offloral bud formation., 1991, 3(7): 677–684.

[27] Yu CW, Liu X, Luo M, Chen C, Lin X, Tian G, Lu Q, Cui Y, Wu K. HISTONE DEACETYLASE6 interacts with flowering locus D and regulates flowering in., 2011, 156(1): 173–184.

[28] Hou XL, Zhou JN, Liu C, Liu L, Shen LS, Yu H. Nuclear factor Y-mediated H3K27me3 demethylation of the SOC1 locus orchestrates flowering responses of., 2014, 5: 4601.

[29] Hisamatsu T, King RW. The nature of floral signals in. II. Roles for FLOWERING LOCUS T (FT) and gibberellin., 2008, 59(14): 3821–3829.

[30] Wang H, Pan J, Li Y, Lou D, Hu Y, Yu D. The DELLA-CONSTANS transcription factor cascade integrates gibberellic acid and photoperiod signaling to regulate flowering., 2016, 172(1): 479– 488.

[31] Aukerman MJ, Sakai H. Regulation of flowering time and floral organ identity by a microRNA and its APETALA2-like target genes., 2003, 15(11): 2730–2741.

[32] Chen X. A microRNA as a translational repressor of APETALA2 inflower development., 2004, 303(5666): 2022–2025.

[33] Mathieu J, Warthmann N, Küttner F, Schmid M. Export of FT protein from phloem companion cells is sufficient for floral induction in., 2007, 17(12): 1055–1060.

[34] Kim JJ, Lee JH, Kim W, Jung HS, Huijser P, Ahn JH. The microRNA156-SQUAMOSA promoter binding protein-like3 module regulates ambient temperature- responsive floweringflowering locus T in., 2012, 159(1): 461–478.

[35] Tiwari SB, Shen Y, Chang HC, Hou Y, Harris A, Ma SF, McPartland M, Hymus GJ, Adam L, Marion C, Belachew A, Repetti PP, Reuber TL, Ratcliffe OJ. The flowering time regulator CONSTANS is recruited to the FLOWERING LOCUS T promotera unique-element., 2010, 187(1): 57–66.

[36] Xu F, Li T, Xu PB, Li L, Du SS, Lian HL, Yang HQ. DELLA proteins physically interact with CONSTANS to regulate flowering under long days in., 2016, 590(4): 541–549.

[37] Kumimoto RW, Adam L, Hymus GJ, Repetti PP, Reuber TL, Marion CM, Hempel FD, Ratcliffe OJ. The Nuclear Factor Y subunits NF-YB2 and NF-YB3 play additive roles in the promotion of flowering by inductive long-day photoperiods in., 2008, 228(5): 709–723.

[38] Cao S, Kumimoto RW, Gnesutta N, Calogero AM, Mantovani R, Holt BF. A distal CCAAT/NUCLEAR FACTOR Y complex promotes chromatin looping at the FLOWERING LOCUS T promoter and regulates the timing of flowering in., 2014, 26(3): 1009–1017.

[39] Davière JM, Achard P. A pivotal role of DELLAs in regulating multiple hormone signals., 2016, 9(1): 10–20.

[40] Fernández V, Takahashi Y, Le Gourrierec J, Coupland G. Photoperiodic and thermosensory pathways interact through CONSTANS to promote flowering at high temperature under short days., 2016, 86(5): 426–440.

[41] Kumar SV, Lucyshyn D, Jaeger KE, Alós E, Alvey E, Harberd NP, Wigge PA. Transcription factor PIF4 controls the thermosensory activation of flowering., 2012, 484(7397): 242–245.

[42] Feng S, Martinez C, Gusmaroli G, Wang Y, Zhou J, Wang F, Chen L, Yu L, Iglesias-Pedraz JM, Kircher S, Schäfer E, Fu X, Fan LM, Deng XW. Coordinated regulation ofthaliana development by light and gibberellins., 2008, 451(7177): 475–479.

[43] Galvão VC, Collani S, Horrer D, Schmid M. Gibberellic acid signaling is required for ambient temperature- mediated induction of flowering in., 2015, 84(5): 949–962.

[44] Li KL, Yu RB, Fan LM, Wei N, Chen HD, Deng XW. DELLA-mediated PIF degradation contributes to coordination of light and gibberellin signalling in., 2016, 7: 11868.

[45] Park J, Nguyen KT, Park E, Jeon JS, Choi G. DELLA proteins and their interacting RING Finger proteins repress gibberellin responses by binding to the promotersof a subset of gibberellin-responsive genes in., 2013, 25(3): 927–943.

[46] Nguyen KT, Park J, Park E, Lee I, Choi G. TheRING domain protein BOI inhibits floweringCO-dependent and CO-independent mechanisms., 2015, 8(12): 1725–1736.

[47] Li MZ, An FY, Li WY, Ma MD, Feng Y, Zhang X, Guo HW. DELLA proteins interact with FLC to repress flowering transition., 2016, 58(7): 642–655.

[48] Jang S, Torti S, Coupland G. Genetic and spatial interactions between FT, TSF and SVP during the early stages of floral induction in., 2009, 60(4): 614–625.

[49] Song YH, Lee I, Lee SY, Imaizumi T, Hong JC. CONSTANS and ASYMMETRIC LEAVES 1 complex is involved in the induction of FLOWERING LOCUS T in photoperiodic flowering in., 2012, 69(2): 332–342.

[50] Zhu Y, Lu L, Shen LS, Yu H. NaKR1 regulates long-distance movement of FLOWERING LOCUS T in., 2016, 2(6): 16075.

[51] Regnault T, Davière JM, Wild M, Sakvarelidze-Achard L, Heintz D, Carrera Bergua E, Lopez Diaz I, Gong F, Hedden P, Achard P. The gibberellin precursor GA12 acts as a long-distance growth signal in., 2015, 1(6): 15073.

[52] Tal I, Zhang Y, Jørgensen ME,Pisanty O, Barbosa IC, Zourelidou M, Regnault T, Crocoll C, Olsen CE, Weinstain R, Schwechheimer C, Halkier BA, Nour- Eldin HH, Estelle M, Shani E. TheNPF3 protein is a GA transporter., 2016, 7: 11486.

[53] Sharma N, Xin R, Kim DH, Sung S, Lange T, Huq E. NO FLOWERING IN SHORT DAY (NFL) is a bHLH transcription factor that promotes flowering specifically under short-day conditions in., 2016, 143(4): 682–690.

[54] Andrés F, Porri A, Torti S, Mateos J, Romera-Branchat M, García-Martínez JL, Fornara F, Gregis V, Kater MM, Coupland G. SHORT VEGETATIVE PHASE reduces gibberellin biosynthesis at theshoot apex to regulate the floral transition., 2014, 111(26): E2760–E2769.

[55] Li D, Liu C, Shen LS,Wu Y, Chen HY, Robertson M, Helliwell CA, Ito T, Meyerowitz E, Yu H. A repressor complex governs the integration of flowering signals in., 2008, 15(1): 110–120.

[56] Achard P, Herr A, Baulcombe DC, Harberd NP. Modu­lation of floral development by a gibberellin-regulated microRNA., 2004, 131(14): 3357–3365.

[57] Blazquez M, Green R, Nilsson O, Sussman MR, Weigel D. Gibberellins promote flowering ofby activating the LEAFY promoter., 1998, 10(5): 791–800.

[58] Blázquez M, Weigel D. Integration of floral inductive signals in., 2000, 404(6780): 889– 892.

[59] Gocal GFW, Sheldon CC, Gubler F, Moritz T, Bagnall DJ, MacMillan CP, Li SF, Parish RW, Dennis ES, Weigel D, King RW. GAMYB-like genes, flowering, and gibberellin signaling in., 2001, 127(4): 1682–1693.

[60] Moon J, Suh SS, Lee H, Choi KR, Hong CB, Paek NC, Kim SG, Lee I. The SOC1 MADS-box gene integrates vernalization and gibberellin signals for flowering in., 2003, 35(5): 613–623.

[61] Jung JH, Seo PJ, Ahn JH,Park CMRNA- binding protein FCA regulates microRNA172 processing in thermosensory flowering., 2012, 287(19): 16007–16016.

[62] Xu J, Hou N, Han N, Bian HW, Zhu MY. The regulatory roles of small RNAs in phytohormone signaling pathways., 2016, 38(5): 418–426.许佳, 侯宁, 韩凝, 边红武, 朱睦元. 小分子RNA在植物激素信号通路中的调控功能. 遗传, 2016, 38(5): 418–426.

[63] Wang JW, Czech B, Weigel D. miR156-regulated SPL transcription factors define an endogenous flowering pathway in., 2009, 138(4): 738–749.

[64] Wu G, Park MY, Conway SR, Wang JW, Weigel D, Poethig RS. The sequential action of miR156 and miR172 regulates developmental timing in., 2009, 138(4): 750–759.

[65] Hyun Y, Richter R, Vincent C, Martinez-Gallegos R, Porri A, Coupland G. Multi-layered regulation of SPL15 and cooperation with SOC1 integrate endogenous flowering pathways at theshoot meristem., 2016, 37(3): 254–266.

[66] Park J, Oh DH, Dassanayake M, Nguyen KT, Ogas J, Choi G, Sun TP. Gibberellin signaling requires chromatin remodeler PICKLE to promote vegetative growth and phase transitions., 2017, 173(2): 1463– 1474.

[67] Zhang D, Jing YJ, Jiang ZM, Lin RC. The chromatin- remodeling factor PICKLE integrates brassinosteroid and gibberellin signaling during skotomorphogenic growth in., 2014, 26(6): 2472– 2485.

[68] Schwab R, Palatnik JF, Riester M, Schommer C, Schmid M, Weigel D. Specific effects of microRNAs on the plant transcriptome., 2005, 8(4): 517–527.

[69] Xu ML, Hu TQ, Zhao JF, Park MY, Earley KW, Wu G, Yang L, Poethig RS. Developmental functions of miR156-regulated SQUAMOSA PROMOTER BINDING PROTEIN-LIKE (SPL) genes inthaliana., 2016, 12(8): e1006263.

[70] Yamaguchi N, Winter CM, Wu MF, Kanno Y, Yamaguchi A, Seo M, Wagner D. Gibberellin acts positively then negatively to control onset of flower formation in., 2014, 344(6184): 638–641.

[71] Turner JG, Ellis C, Devoto A. The jasmonate signal pathway., 2002, 14(Suppl.): S153–164.

[72] Berger S. Jasmonate-related mutants ofas tools for studying stress signaling., 2002, 214(4): 497–504.

[73] Liu X, Yu CW, Duan J, Luo M, Wang K, Tian G, Cui Y, Wu K. HDA6 directly interacts with DNA methyl­transferase MET1 and maintains transposable element silencing in., 2012, 158(1): 119–129.

[74] Yu CW, Liu XC, Luo M, Chen C, Lin XD, Tian G, Lu Q, Cui YH, Wu KQ. HISTONE DEACETYLASE6 interacts with flowering locus D and regulates flowering in., 2011, 156(1): 173–184.

[75] He YH, Michaels SD, Amasino RM. Regulation of flowering time by histone acetylation in., 2003, 302(5651): 1751–1754.

[76] Ishiguro S, Kawai-Oda A, Ueda J, Nishida I, Okada K. The DEFECTIVE IN ANTHER DEHISCIENCE gene encodes a novel phospholipase A1 catalyzing the initial step of jasmonic acid biosynthesis, which synchronizes pollen maturation, anther dehiscence, and flower opening in., 2001, 13(10): 2191–2209.

[77] Nelson MR, Band LR, Dyson RJ, Lessinnes T, Wells DM, Yang C, Everitt NM, Jensen OE, Wilson ZA. A biomechanical model of anther opening reveals the roles of dehydration and secondary thickening., 2012, 196(4): 1030–1037.

[78] Nagpal P, Ellis CM, Weber H, Ploense SE, Barkawi LS, Guilfoyle TJ, Hagen G, Alonso JM, Cohen JD, Farmer EE, Ecker JR, Reed JW. Auxin response factors ARF6 and ARF8 promote jasmonic acid production and flower maturation., 2005, 132(18): 4107–4118.

[79] Jones-Rhoades MW, Bartel DP. Computational identification of plant micrornas and their targets, including a stress-induced miRNA., 2004, 14(6): 787–799.

[80] Gutierrez L, Bussell JD, Pacurar DI,Schwambach J, Pacurar M, Bellini C. Phenotypic plasticity of adventitious rooting inis controlled by complex regulation of auxin response factor transcripts and microRNA abundance., 2009, 21(10): 3119–3132.

[81] Zhai QZ, Zhang X, Wu FM, Feng HL, Deng L, Xu L, Zhang M, Wang QM, Li CY. Transcriptional mechanismof jasmonate receptor COI1-mediated delay of flowering time in., 2015, 27(10): 2814– 2828.

[82] Dong T, Park Y, Hwang I. Abscisic acid: biosynthesis, inactivation, homoeostasis and signalling., 2015, 58: 29–48.

[83] Barrero JM, Piqueras P, González-Guzmán M, Serrano R, Rodríguez PL, Ponce MR, Micol JL. A mutational analysis of thegene ofhighlights the involvement of ABA in vegetative development., 2005, 56(418): 2071–2083.

[84] Liu T, Longhurst AD, Talavera-Rauh F, Hokin SA, Barton MK. Thetranscription factor ABIG1 relays ABA signaled growth inhibition and drought induced senescence., 2016, 5: e13768.

[85] Conti L, Galbiati M, Tonelli C. ABA and the floral transition. In: Zhang DP, eds. Abscisic acid: metabolism, transport and signaling. Springer, The Netherlands, Dordrecht, 2014, 365–384.

[86] Domagalska MA, Sarnowska E, Nagy F. Davis SJ. Genetic analyses of interactions among gibberellin, abscisic acid, and brassinosteroids in the control of flowering time in., 2010, 5(11): e14012.

[87] Okuda H, Kihara T, Iwagaki I. Effects of cropping on photosynthesis, dark respiration, leaf ABA concentrationand inflorescence induction in., 1995, 64(1): 9–16.

[88] Li JX, Hu CX, Gao JY, Yue JQ. Research progress in floral mechanism and regulation of Citrus., 2012, (3): 67–70.李进学, 胡承孝, 高俊燕, 岳建强. 柑橘成花机理与调控研究进展. 中国果树, 2012, (3): 67–70.

[89] Ma L, Li F, Zhang JB, Wu GF, Chen ZQ, Wang XL, Tan YY, Wang QL. Relationship between flower bud differentiation and endogenous hormones in shoot tip of different upland cotton varieties., 2018, 46(16): 71–75.马亮, 李飞, 张金宝, 吴国峰, 陈宗全, 王晓玲, 谭阳光, 王清连. 不同陆地棉品种花芽分化与茎尖内源激素的关系. 江苏农业科学, 2018, 46(16): 71–75.

[90] Cao SY, Zhang JC, Wei LH. Studies on the changes of endogenous hormones in the differentiation period of flower bud in apple trees., 2000, 17(4): 244–248.曹尚银, 张俊昌, 魏立华. 苹果花芽孕育过程中内源激素的变化. 果树学报, 2000, 17(4): 244–248.

[91] Huang QW. Chang in endogenous hormone contents in relation to bud differention and on-year or off-year fruiting of longan., 1996, 4(2): 58–62.黄羌维. 龙眼内源激素变化和花芽分化及大小年结果的关系. 热带亚热带植物学报, 1996, 4(2): 58–62.

[92] Guo R, Sun GH. Relatonship of endogenesis hormones and dormancy of bulbs and differentiation of buds of lilies., 2007, (5): 41–42, 44.郭蕊, 孙国惠.百合内源激素与鳞茎休眠及花芽分化关系的研究. 辽宁林业科技, 2007, (5): 41–42, 44.

[93] Lin G Y, Zheng CS, Sun XZ, Wang WL. Effects of photoperiod on floral bud differentiation and contents of endogenous hormones in chrysanthemum., 2008, (1): 35–39.林贵玉, 郑成淑, 孙宪芝, 王文莉. 光周期对菊花花芽分化和内源激素的影响. 山东农业科学, 2008, (1): 35–39.

[94] Riboni M, Galbiati M, Tonelli C, Conti L. GIGANTEA enables drought escape responseabscisic acid- dependent activation of the florigens and suppressor of overexpression of constans1., 2013, 162(3): 1706–1719.

[95] Riboni M, Robustelli Test A, Galbiati M, Tonelli C, Conti L. ABA-dependent control of GIGANTEA signalling enables drought escapeup-regulation of FLOWERING LOCUS T in., 2016, 67(22): 6309–6322.

[96] Choi H, Hong J, Ha J, Kang J, Kim SY. ABFs, a family of ABA-responsive element binding factors., 2000, 275(3): 1723–1730.

[97] Uno Y, Furihata T, Abe H, Yoshida R, Shinozaki K, Yamaguchi-Shinozaki K.basic leucine zipper transcription factors involved in an abscisic acid- dependent signal transduction pathway under drought and high-salinity conditions., 2000, 97(21): 11632–11637.

[98] Fujii H, Verslues PE, Zhu JK. Identification of two protein kinases required for abscisic acid regulation of seed germination, root growth, and gene expression in., 2007, 19(2): 485–494.

[99] Fujita Y, Nakashima K, Yoshida T, Katagiri T, Kidokoro S, Kanamori N, Umezawa T, Fujita M, Maruyama K, Ishiyama K, Kobayashi M, Nakasone S, Yamada K, Ito T, Shinozaki K, Yamaguchi-Shinozaki K. Three SnRK2 protein kinases are the main positive regulators of abscisic acid signaling in response to water stress in., 2009, 50(12): 2123– 2132.

[100] Yoshida T, Fujita Y, Maruyama K, Mogami J, Todaka D, Shinozaki K, Yamaguchi-Shinozaki K. FourAREB/ABF transcription factors function predominantly in gene expression downstream of SnRK2 kinases in abscisic acid signalling in response to osmotic stress., 2014, 38(1): 35–49.

[101] Ito S, Song YH, Josephson-Day AR, Miller RJ, Breton G, Olmstead RG, Imaizumi T. Flowering bhlh transc­riptional activators control expression of the photo­periodic flowering regulator constans in., 2012, 109(9): 3582–3587.

[102] Wang F, Zhu DM, Huang X, Li S, Gong YN, Yao QF, Fu XD, Fan LM, Deng XW. Biochemical insights on degradation ofDELLA proteins gained from a cell-free assay system., 2009, 21(8): 2378–2390.

[103] Yu FF, Xie Q. Ubiquitination modification precisely modulates the ABA signaling pathway in plants., 2017, 39(8): 692–706.于菲菲, 谢旗. 泛素化修饰调控脱落酸介导的信号途径. 遗传, 2017, 39(8): 692–706.

[104] Zhang X, Garreton V, Chua NH. The AIP2 E3 ligase acts as a novel negative regulator of ABA signaling by promoting ABI3 degradation., 2009, 276(13): 1532–1543.

[105] Bao SJ, Hua CM, Huang JQ, Cheng P, Gong XM, Shen LS, Yu H. Molecular basis of natural variation in photoperiodic flowering responses., 2019, 50(1): 90–101.e3.

[106] Wang YP, Li L, Ye TT, Lu YM, Chen X, Wu Y. The inhibitory effect of ABA on floral transition is mediated by ABI5 in., 2013, 64(2): 675– 684.

[107] Shu K, Chen Q, Wu YR, Liu RJ, Zhang HW, Wang SF, Tang SY, Yang WY, Xie Q. ABSCISIC ACID- INSENSITIVE 4 negatively regulates flowering through directly promotingtranscription., 2016, 67(1): 195–205.

[108] Johnson PR, Ecker JR. The ethylene gas signal transduction pathway: a molecular perspective., 1998, 32(1): 227–254.

[109] Frankowski K, Wilmowicz E, Kućko A, Kęsy J, Świeżawska B, Kopcewicz J. Ethylene, auxin, and abscisic acid interactions in the control of photoperiodic flower induction in., 2014, 58(2): 305–310.

[110] Achard P, Baghour M, Chapple A,Hedden P, Van Der Straeten D, Genschik P, Moritz T, Harberd NP. The plant stress hormone ethylene controls floral transitionDELLA-dependent regulation of floral meristem- identity genes., 2007, 104(15): 6484–6489.

[111] Alonso JM, Ecker JR. The ethylene pathway: a paradigm for plant hormone signaling and interaction., 2001, (70): re1.

[112] Zhou CH, Zhang L, Duan J, Miki B, Wu KQ. HISTONE DEACETYLASE19 is involved in jasmonic acid and ethylene signaling of pathogen response in., 2005, 17(4): 1196–1204.

[113] Mai YX, Wang L, Yang HQ. A gain-of-function mutation in IAA7/AXR2 confers late flowering under short-day light in., 2011, 53(6): 480–492.

[114] Jaligot E, Rival A, Beulé T, Dussert S, Verdeil JL. Somaclonal variation in oil palm (Elaeis guineensis Jacq.): the DNA methylation hypothesis., 2000, 19(7): 684–690.

[115] Cheng YF, Zhao YD. A role for auxin in flower development., 2007,49(1): 99–104.

[116] Reinhardt D, Mandel T, Kuhlemeier C. Auxin regulates the initiation and radial position of plant lateral organs., 2000, 12(4): 507–518.

[117] Przemeck GK, Mattsson J, Hardtke CS, Sung ZR, Berleth T. Studies on the role of the Arabidopsis gene MONOPTEROS in vascular development and plant cell axialization., 1996, 200(2): 229–237.

[118] Krizek BA, Eaddy M. AINTEGUMENTA-LIKE6 regulates cellular differentiation in flowers., 2012, 78(3): 199–209.

[119] O'Neill DP, Ross JJ. Auxin regulation of the gibberellin pathway in pea., 2002, 130(4): 1974–1982.

[120] Frigerio M, Alabadí D, Pérez-Gómez J, García-Cárcel L, Phillips AL, Hedden P, Blázquez MA. Transcriptional regulation of gibberellin metabolism genes by auxin signaling in., 2006, 142(2): 553–563.

[121] Fu X, Harberd NP. Auxin promotes Arabidopsis root growth by modulating gibberellin response., 2003, 421(6924): 740–743.

[122] Perilli S, Moubayidin L, Sabatini S. The molecular basis of cytokinin function., 2010, 13(1): 21–26.

[123] Jacqmard A, Gadisseur I, Bernier G. Cell division and morphological changes in the shoot apex ofduring floral transition., 2003, 91(5): 571–576.

[124] Bartrina I, Otto E, Strnad M, Werner T, Schmülling T. Cytokinin regulates the activity of reproductive meristems, flower organ size, ovule formation, and thus seed yield in., 2011, 23(1): 69–80.

[125] Corbesier L, Prinsen E, Jacqmard A, Lejeune P, Van Onckelen H, Périlleux C, Bernier G. Cytokinin levels in leaves, leaf exudate and shoot apical meristem ofduring floral transition., 2003, 54(392): 2511–2517.

[126] Bernier G, Corbesier L, Périlleux C. The flowering process: on the track of controlling factors in sinapis alba., 2002, 49(4): 445–450.

[127] Meijón M, Cañal M J, Valledor L, Rodríguez R, Feito I. Epigenetic and physiological effects of gibberellin inhibitors and chemical pruners on the floral transition of azalea., 2011, 141(3): 276–288.

[128] Lee TT, Skoog F. Effects of substituted phenols on bud formation and growth of tobacco tissue cultures., 1965, 18(2): 386–402.

[129] Cleland CF, Ajami A. Identification of the flower- inducing factor isolated from aphid honeydew as being salicylic acid., 1974, 54(6): 904–906.

[130] Khurana JP, Cleland CF. Role of salicylic acid and benzoic acid in flowering of a photoperiod-insensitive strain, Lemna paucicostata LP6., 1992, 100(3): 1541–1546.

[131] Wada KC, Yamada M, Shiraya T,Takeno K. Salicylic acid and the flowering gene flowering locus T homolog are involved in poor-nutrition stress-induced flowering of., 2010, 167(6): 447– 452.

[132] Wada KC, Takeno K. Stress-induced flowering., 2010, 5(8): 944–947.

[133] Martínez C, Pons E, Prats G, León J. Salicylic acid regulates flowering time and links defence responses and reproductive development., 2004, 37(2): 209–217.

Progress on the mechanism of hormones regulating plant flower formation

Liping Zou, Cheng Pan, Mengxin Wang, Lin Cui, Baoyu Han

Flowering is the adaptability of plants in response to the environment, which is regulated by the complex flowering control network formed by a variety of exogenous and endogenous signals. Plant hormones, the most important endogenous signal participants, play important roles in the process of plant flowering. Recent reports reveal the pivotal roles of hormones in the epigenetic regulation and flowering promotion pathway. In addition, synergistic or antagonistic interaction has been observed among many hormones. Numerous hormones have been found to be involved in the regulation of the multiple flowering development regulation and signaling pathways mediated by DELLA protein in the gibberellin (GA) pathway. In this review, we summarize the recent advances ofthe flowering mechanisms related to GA pathway and discuss the effects of abscisic acid (ABA), auxin (IAA), cytokinin (CTK), salicylic acid (SA), jasmonic acid (JA), and ethylene (ET) on flowering, including their cross-regulation with DELLA, miRNAs, and transcription factor (TFs). This review provides a reference for further comprehensive analysis of the hormone-regulated network of plant flower formation.

plant hormone; flower bud differentiation; floral regulation; signal transduction

2020-01-13;

2020-03-11

国家重点研发计划项目(编号：2018YFC1604402)，浙江省重点研发计划项目(编号：2020C02026)和浙江省基础公益研究计划项目(编号：LGN18C160006，LGN20C140005)资助[Supported by the National Key Research and Development Program of China (No. 2018YFC1604402), the Zhejiang Provincial Key Research and Development Program of China (No.2020C02026), and the Zhejiang Provincial Fundamental and Public Welfare of China (Nos. LGN18C160006, LGN20C140005)]

邹礼平，在读硕士研究生，专业方向：生物化学与分子生物学。E-mail: 1223760931@qq.com

韩宝瑜，博士，教授，研究方向：化学生态与分子生物学。E-mail: hanby15@163.com

10.16288/j.yczz.20-014

2020/4/16 9:17:22

URI: http://kns.cnki.net/kcms/detail/11.1913.R.20200416.0846.002.html

(责任编委: 李传友)