全 文 ：植物生理学报 Plant Physiology Journal 2014, 50 (10): 1459~1468　　doi: 10.13592/j.cnki.ppj.2014.0270 1459
收稿 2014-06-10　　修定 2014-09-15
资助 中国农业科学院基本科研业务费预算增量项目(2013ZL018)
和国家自然科学基金项目(31301754)。
* 通讯作者(E-mail: zhanghongjum@caas.cn; Tel: 0429-3598198)。
高等植物成花诱导调控的分子和遗传机制
宋杨, 窦连登, 张红军*
中国农业科学院果树研究所, 农业部园艺作物种质资源利用重点实验室, 辽宁兴城125100
摘要: 成花诱导是高等植物由营养生长向生殖生长过渡的重要环节。成花诱导过程由内因和外因两个因素决定。近年来,
在对拟南芥、水稻等有花模式植物成花机制的研究中, 已发现植物成花主要受春化、温敏、光周期、赤霉素、自主、成
花抑制和年龄7条途径控制。文章简要综述这7条途径相关研究的最新进展, 以期为今后从分子和生理水平调控植物成花
诱导提供基础。
关键词: 高等植物; 成花诱导; 分子和遗传机制
Molecular and Genetic Mechanisms of Control of Floral Induction in Higher Plants
SONG Yang, DOU Lian-Deng, ZHANG Hong-Jun*
Key Laboratory of Horticultural Crops Germplasm Resources Utilization, Ministry of Agriculture, Research Institute of Pomology,
Chinese Academy of Agricultural Sciences, Xingcheng, Liaoning 125100, China
Abstract: Floral induction represents a crucial transition from the vegetative stage to the reproductive stage in
higher plants. This process is determined by both environmental and endogenous factors. The regulating mech-
anisms of flowering pathways have been studied extensively in Arabidopsis thaliana, Oryza sativa and several
flowering plants. Seven pathways, vernalization pathway, thermosensory pathway, photoperiod pathway, gib-
berellin (GA) pathway, autonomous pathway, repression pathway and aging pathway were involved in flower-
ing control. This review summarizes recent progresses in controlled flowering time, and provides a foundation
for molecular and physiological research on floral control.
Key words: higher plants; floral induction; molecular and genetic mechanisms
高等植物成花过程包括成花诱导(floral induc-
tion)、成花启动(floral evocation)和花的发育(floral
development) 3个阶段, 这一过程受植物自身遗传
和外界环境共同调控决定。其中, 成花诱导指植
物从营养生长向生殖生长转变的过程, 对成花过
程起关键作用。不同植物的成花诱导过程有一定
的相似性, 如光照会诱导植物产生成花信号而使
植物进行成花转变。近些年, 随着拟南芥(Arabi-
dopsis thaliana)、水稻(Oryza sativa)等模式植物全
基因组序列测定完成, 对其成花诱导分子机制进
行了大量研究工作并取得了一定进展。在植物成
花过程中, 受温度、光和激素等许多因素影响, 并
明确了高等植物的7条成花诱导途径, 即春化途
径、温敏途径、光周期途径、赤霉素(gibberellin,
GA)途径、自主途径、成花抑制途径和年龄途
径。本文以拟南芥等开花模式植物为主, 综述近
些年植物成花诱导的研究进展, 为进一步调控植
物成花诱导提供理论依据。
1 春化途径
春化作用是温带地区植物发育过程中表现出
来的特征, 指植物需要一定时间和特定低温的处
理, 才能开花的现象, 这种低温促进植物开花的作
用称为春化作用。目前, 研究者们已发现一些在
春化途径中调控植物成花的关键基因。隶属
MADS-box基因家族的FLC (FLOWERING LOCUS
C)转录因子是近些年关于春化作用研究的热点之
一。在拟南芥中有5个FLC旁系同源基因, 它们反
向调节拟南芥成花, 从而抑制成花转变(Koornneef
等1994; Sheldon等1999; Searle等2006; Helliwell等
2011)。FLC可以与SOC1 (SUPPRESSOR OF OVER-
EXPRESSION OF CONSTANS 1)和FT (FLOWERING
LOCUS T)的CArG区域结合而抑制其表达, 进而抑
植物生理学报1460
制成花(Hepworth等2002; Helliwell等2006; Deng等
2011)。甜菜(Beta vulgaris spp. vulgaris)中的BvFT1
也可以抑制开花, 它的表达量高低对于甜菜能否
响应春化作用十分关键, 当BvFT1下调表达时, 甜
菜才能感应低温而表现开花, 这与FT在拟南芥中
的作用方式不同(Pin等2010)。FT的表达还受到具
有AP2结构域的RAV基因家族的调节(Aukerman和
Sakai 2003)。TEM1 (TEMPOANILLO 1)、TEM2、
APETALA2、SMZ (SCHLAFMUTZE)、ANAR-
CHZAPFEN、TOE1 (TARGET OF EAT 1)、TOE2和
TOE3都属于RAV基因家族, 它们是miR172的靶基
因(Kim等2006; Mathieu等2009; Yant等2010)。超
量表达这些基因可以使转基因植株延迟开花, 这
说明它们是植株开花的抑制子。进一步研究显示,
TEM1和SMZ可以与FT相互作用, 进而抑制FT的表
达(Castillejo和Pelaz 2008)。FLC的表达还受FRI
(FRIGIDA)的调节, FLC和FRI可以共同调控植物成
花诱导, 但它们的作用机制还不清楚, 推测FRI能
与FLC互作, 从而上调FLC的表达(Geraldo等2009;
Choi等2011)。水稻的FT同源基因Hd3a可通过嫁
接的方法转移到其他组织中(Tamaki等2007; Na-
varro等2011)。温度变化可通过光敏色素作用因子
PIF4 (PHYTOCHROME INTERACTING FACTOR
4)激活FT的表达(Kumar等2012)。VRN (VERNAL-
IZATION)类基因也是与春化作用相关的基因, 它
们能抑制FLC的表达而促进成花(Gendall等2001;
Levy等2002; Chen和Dubcovsky 2012) (图1)。
近些年, 随着表观遗传学的研究, 人们发现春
化途径还跟DNA甲基化、组蛋白的甲基化和乙酰
化相关, 低温处理可以增加FLC染色质组蛋白的去
乙酰化(He等2003; Bastow等2004; Buzas等2011;
Xu等2013)。使用DNA甲基化抑制剂处理, 可使拟
南芥基因组的甲基化程度降低, 从而使FLC的表达
下调而促进植株开花(Finnegan等1998)。春化作用
使FLC发生沉默, 进而促进植株提前开花。深入研
究发现, 春化作用可以诱导VIN3 (VERNALIZA-
TION-INSENSITIVE 3)表达 , VIN3可与PRC2
(PHD-polycomb repressive complex 2)相互作用, 进
而使FLC基因座发生三甲基化修饰(Finnegan和
Dennis 2007; de Lucas等2008)。VIN3主要作用是
对FLC的抑制, VIN1和VIN2的功能是维持对FLC的
抑制。在拟南芥vin3突变体中, FLC的表达不受春
化作用的影响, 推测VRN1和VRN2能够维持FLC的
抑制状态(Wang等2009)。在拟南芥中, 过量表达
去甲基化酶JMJ18 (JUMONJIC 18)能使转基因植
株早开花, 推测是由于JMJ18直接与FLC互作而抑
制了FLC的表达, 从而启动了FT的转录表达, 最终
使植物表现早花(Yang等2012)。FLC还可以直接
调控影响植物童期长短的基因, 说明FLC在调控植
株由营养生长向生殖生长转变的过程中起一定作
用(Willmann和Poethig 2011)。FLC组蛋白的修饰
对植株花期的控制起关键作用, 当FLC组蛋白H3
第4位氨基酸处于甲基化修饰状态, 或第9和27位
氨基酸处于甲基化状态时, FLC分别处于激活状态
和抑制状态。进一步研究发现, PRC2具有组蛋白
甲基转移酶活性, 可以催化FLC组蛋白H3第27位
氨基酸的三甲基化(Zhang等2009; Yang等2013)。
FLC组蛋白H4第5位氨基酸的乙酰化程度降低, 可
维持FLC表达的抑制状态, 使植株能够正常开花
(Kim等2013; Xiao等2013)。
综上, 适当低温能够促进植物成花转变, 植物
把冷信号传递给网络通络上的多种基因, 这些基
因通过上调、抑制FLC的转录活性或FLC发生表
观调控, 从而影响植物的成花诱导。另外, 拟南芥
中miR172表达量的高低, 可以调控拟南芥对温度
的敏感度, 超量表达miR172时, 转基因植株表现为
早花。进一步研究发现, miR172调控的靶基因是
AP2 (APETAIA 2)-like, 它抑制AP2的表达从而调控
植物成花(Aukerman和Sakai 2003; Lee等2010; Ji等
2011)。
2 温敏途径
植物在营养生长时期所处的外界环境温度也
能影响植株成花转变。MADS-box蛋白家族的SVP
(SHORT VEGETATIVE PHASE)是温敏途径中的关
键基因。SVP可以与FT和SOC1基因启动子区域的
CArG序列相结合(Lee等2007), 还可与miR172启动
子区域的CArG序列结合, 从而直接调控miR172的
转录(Cho等2012)。SVP也能分别在植株的营养生
长和生殖生长阶段与FLC和AP1互作, 从而调控植
株开花(Gregis等2013)。SVP可以介导GA途径, 通
过抑制植株GA的生物合成而调控成花(Andrés等
2014)。拟南芥在短日照25~27 ℃下, 比在长日照
宋杨等: 高等植物成花诱导调控的分子和遗传机制 1461
23 ℃下的花期提前。fri和flc缺失型突变体在27 ℃
条件下比在23 ℃下花期提前, 经证明FLC在温敏
途径中起抑制作用(Werner等2005)。FLM (FLOW-
ERING LOCUS M)也是温敏途径中的重要基因, 它
与FLC具有较高的同源性, 植株在营养生长时期的
环境温度可影响FLM mRNA前体的可变剪切位点
(Balasubramanian等2006)。温敏途径中的另一个
关键蛋白是ARP6 (ACTIN-RELATED PROTEIN
6), 它通过维持FLC的表达而抑制开花(Choi等
2005; Deal等2005)。
3 光周期途径
光周期是影响植物生长发育的重要条件之一,
其直接作用是指对植物形态建成的作用。光周期
是调节植物成花诱导的重要环境因子。对光周期
敏感的植物, 只有在适宜的光周期条件下才能成
花, 而长日照植物和短日照植物对光周期的要求
不同。拟南芥是长日照植物, 其光周期途径起始
于光受体对不同光周期和光质的感应。拟南芥中
光受体包括光敏色素(phytochrome, PHY)、隐花色
素(cryptochrome, CRY)、向光素(phototropin,
PHOT)和UV-B受体。光敏色素能感应红光和远红
光, 隐花色素和向光素感应UV-A、蓝光和紫外光,
UV-B受体能够感应UV-B。在拟南芥中有5种光敏
色素(PHY A~E)和3种隐花色素(CRY 1~3) (Furuya
和Schäfer 1996), 它们可感受光周期的长短和光质
的异同。在短日照条件下, PHYA的表达可能受
AIL1~4 (AINTEGUMENTA-like)的调节, 进而改变
了PHYA对红光和远红光的敏感性(Karlberg等
图1 拟南芥中成花诱导调控途径
Fig.1 The floral induction pathways in Arabidopsis
参照孙昌辉等(2007)文献修改。
植物生理学报1462
2011)。拟南芥中的光敏色素和隐花色素能把光信
号传递进入生物钟, 以纠正植物体中的时间误差
(Devlin 2002; Fankhauser和Staiger 2002), 植株通过
UV-B受体接受低强度的UV-B, 从而启动生物钟调
控中CCA1 (CIRCADLAN CLOCK ASSOCIATED 1)
等关键基因的表达。拟南芥的UV-B受体还可以与
光信号转导途径中的关键蛋白COP1相互作用, 进
而调控植株光形态发生。进一步研究发现, 植株
经UV-B处理后, UV-B受体可与COP1发生互作,
COP1的WD40结构域在互作过程中起关键作用
(Favory等2009; Rizzini等2011)。
影响光周期的另一个重要内容是昼夜节律。
Takano等(2005)发现, 影响植物昼夜节律的一些基
因发生突变而形成的突变体, 在光周期发生变化
时, 其昼夜节律平衡会被破坏, 继而影响植物成
花。在拟南芥中影响昼夜节律的基因包括CCA1和
LHY (LATE ELONGA TED HYPOCOTYL)。PHYB
在感受到光信号后, 与PIF3结合, 进而上调CCA1和
LHY的表达水平, 从而影响植株对光周期变化的感
应(Martínez-García等2000; Hemmes等2012)。
植物感受光周期变化刺激的部位不是茎尖的
生长点而是叶片。CO (CONSTANS)基因是光周期
途径中植物成花诱导过程中的关键基因, CCA1和
LHY等基因的表达可以激活叶片中CO的表达
(Ayre和Turgeno 2004), 而GI (GIGANTEA)可协调
CO基因与CCA1和LHY基因之间的作用功能(Doyle
等2002; Sawa和Kay 2011)。GI的转录水平也受昼
夜节律的调控, 其功能缺失型突变体的GI基因转
录被破坏, 使突变体不能正常感应光周期的变化
(Fowler等1999)。拟南芥bHLH转录因子FBH也可
以正向调节CO基因 , 从而调控成花诱导(Ito等
2012)。在春化途径中提到的FT基因也是植物成
花诱导光周期途径中的关键基因。Wigge等(2005)
研究发现, 通过嫁接普通型拟南芥和FT功能缺失
型突变体的方法 , 能使突变体正常成花。Li等
(2011)进一步研究发现, 拟南芥FT mRNA还可独立
于FT蛋白而移动到茎顶端分生组织中, 这种未经
过翻译过程的FT mRNA可以在短日照条件下启动
成花。同样, 在豌豆(Pisum sativum)和玉米(Zea
mays)中FT的同源基因也可以启动植株在光周期
调控下开花(Hecht等2011; Meng等2011)。FT的表
达还受CO基因的调控, CO可以激活FT的转录活性
而促进拟南芥成花(Samach等2000; Valverde等
2004)。FT还能与PC (PHOSPHATIDYLCHOLINE)
相互作用而启动拟南芥成花(Nakamura等2014)。
HOS1 (HIGH EXPRESSION OF OSMOTICALLY
RESPONSIVE GENES 1)编码一个泛素连接酶E3,
它也能与CO基因互作, 在长日照条件下调控FT的
转录(Lazaro等2012)。
4 GA途径
许多植物激素都与植物的成花诱导相关, 如
GA、生长素、脱落酸和多胺等。GA是在成花调
控中研究得较多和深入的一种植物内源激素。GA
并不是独立调控植物成花诱导, 其他激素也能够
与GA相互渗透, 共同调控植物成花(Yamaguchi等
2013)。GA对不同植物成花具有明显不同的影
响。外施GA时, 促使一些长日照植物在短日照条
件下成花, 而且不同种类的GA (如GA3、GA4和
GA7)对于同一植物的成花诱导具有不同的活性。
如GA4对苹果(Malus domestica)成花有促进作用,
而GA3有抑制作用(李合生2005)。
近年来, 随着研究的深入, 研究者发现植物体
内GA合成受阻或植物体不能感应GA, 都能导致植
物体内GA含量或活性发生变化。这可能是由于
GA合成代谢途径或GA信号转导途径中一些基因
突变造成的。在许多植物中都存在GA缺陷性突变
体, 这种突变体中GA的合成受阻或代谢过量, 都会
导致植物体内源GA缺乏, 使植物表现晚花和矮化
等表型(Spielmeyer等2002; Magome等2008)。一些
响应GA的基因发生突变而形成的GA不敏感型突
变体, 如gai (gibberellic acid insensitive)、rga 1~3
(repressor of ga 1~3)和rgl1 (rga-like 1), 这些突变体
中的突变基因所编码的蛋白均属于典型的GRAS
蛋白家族, 具有DELLA和VHYNP结构域, 它们的
功能缺失型突变体表现为使植物早花。GA可以通
过DELLA蛋白调控早花基因LEAFY, 从而促进
LEAFY的表达, 而RGA功能缺失型突变体则不能正
常表达LEAFY (Blázquez等1998)。进一步研究发
现, GA通过解除DELLA对转录因子SPL (SQUA-
MOSA PROMOTER BINDING-LIKE)的抑制作用,
而激活MADS box基因和miR172, 从而调控开花时
间(Yu等2012)。超量表达RGL1蛋白的植株表现为
宋杨等: 高等植物成花诱导调控的分子和遗传机制 1463
雄蕊、花瓣发育不完全和雄性不育。当这些蛋白
的DELLA结构域突变后, 这种现象就会被阻止
(Dill和Sun 2001)。因此, DELLA功能域的改变可
能会造成植物对GA的响应, 将缺少DELLA区域的
RGL1蛋白过量表达, 转基因植株表现出与GA合成
缺陷型突变体相同的表型(Wen和Chang 2002)。
DELLA蛋白还能直接调控PIF基因, 从而间接调控
F T的表达 , 进而调控成花 ( d e L u c a s等2 0 0 8 ;
Schwechheimer和Willige 2009)。拟南芥miR159在
GA途径中起重要作用, miR159a过量表达的植株
表现为在短日照条件下花期延迟, 在长日照条件
下花期没有变化(Achard等2004)。miR159的靶基
因大多是MYB类转录因子, 超量表达miR159a的株
系中, MYB33和MYB65的表达量均下降, 而miR-
159ab双突变体中, MYB33和MYB65都上调表达, 突
变体花期晚于野生型植株。DELLA通过抑制
miR159而间接调控MYB33、MYB65和MYB101的
表达, 从而控制LFY的转录, 继而调控植株开花时
间(Park等2002; Palatnik等2003; Achard等2004)。
5 自主途径
自主途径指在外界环境条件不适合植物开花
的情况下, 植物体在自身营养生长达到一定阶段
时能够自主开花的现象。研究者将在长日照和短
日照条件下都表现晚花的突变体称为自主途径类
突变体。从拟南芥突变体中筛选到一些调控自主
途径的基因, 如FCA和FPA等。这些基因均可通过
抑制FLC的表达, 从而促进植物成花(Michaels和
Amasino 2001)。FCA属于RNA结合类基因, 它编
码2个RNA结合域, 其mRNA的前体能被剪切为4
种不同的转录产物, 并可以自主调控(Macknight等
1997; Macknight等2002; Quesada等2003)。FCA也
可以调控FLC的表达(Feng等2011)。FPA与FCA的
结构相似, 其N-端也有RNA识别结构域, 能与FLC
互作, 进而调控FLC的表达(Schombury等2001;
Hornyik等2010)。FLD (FLOWERING LOCUS D)
基因编码的蛋白与赖氨酸去甲基化酶LSD1高度同
源, FVE基因编码一个MSI1的同源基因, 它们均与
组蛋白脱乙酰化复合体的形成相关。FLD和FVE
编码的蛋白与人类去乙酰化酶HDAC高度同源, 对
FLC组蛋白起到去乙酰化作用, 而使FLC发生沉
默。FLD和FVE的功能缺失会使植株发生晚花现
象, 深入研究发现, fld和fve突变体中FLC的H4乙酰
化水平比野生型高, 因而发生花期推迟(He等2003;
He和Amasino 2005)。在野生型拟南芥中, flc功能
缺失型突变体表现为抑制自主途径类突变体的晚
花现象, 这也说明自主途径是通过FLC基因来调控
成花(Michaels和Amasino 2001)。根据以上研究结
果可以推测, 自主途径与春化途径基因网络的节
点可能是FLC基因, 植物均通过控制FLC的表达来
调控成花转变。
6 成花抑制途径
在拟南芥中, 一些突变体植株表现为开花极
早, 营养生长缓慢, 或者不经过任何营养生长, 在
种子萌发后在子叶表面直接生长出柱头乳突等生
殖器官。这说明某些基因在开花调控中起抑制作
用。EMF (EMBRYO FLOWER)基因被认为在这种
突变体中主要起抑制开花的作用(Haung和Yang
1998)。在普通型植株中, 随着植物的生长发育,
EMF对开花的抑制作用表现为逐渐降低, 当这种
抑制作用降低到一定程度时, 植物开始从营养生
长转向生殖生长(Chou等2001)。推测EMF基因可
能通过抑制花分生组织基因AP1 (APETAIA 1)和
AG (AGMAMOUS)的表达而抑制成花转变。
TFL1 (TERMINAL FLOWER 1)是另一个成花
抑制因子, TFL1与FT高度同源, 但功能却不相同,
tfl1功能缺失型突变体与FT超量表达植株的表型十
分相似(Hanano和Goto 2011)。tfl1突变体表现为开
花早 , 茎顶端分生组织停止生长 , 茎顶端成花
(Shannon和Meeks-Wagner 1991)。在幼苗阶段生
长的拟南芥中, 通过TFL1对LFY的抑制作用而调控
成花(Wang等2011)。CLF (CURLY LEAF)和WLC
(WAVYLEAVES AND COTYLEDONS)与EMF的功能
相似, 在clf突变体中, AG基因的相对表达量升高,
而wlc突变体中AP3的表达量升高 , 说明CLF和
WLC也是通过抑制AP3和AG基因的表达来调控成
花转变(Kim等1998)。
7 年龄途径
植物在从幼年到成年的整个生命周期中 ,
miR156在植株对年龄响应中起关键作用。在植株
的幼年期, miR156高度表达, 其表达量随着植株年
龄的增长而逐渐减少; 而miR172的表达模式与
miR156相反, 表达量随着植株年龄增加而表现上
植物生理学报1464
升(Wang等2009; Wu等2009)。过量表达miR156会
使转基因植株表现幼态化, 而过量表达miR172可
使植株提早进入成年期(Wu和Poethig 2006; Xie等
2006; Chuck等2007)。用糖处理植株, 可以减少植
株体内miR156的含量, 进一步研究表明, 糖处理既
能在转录水平抑制miR156前体的转录, 又在转录
后水平诱导miR156前体的降解。这说明糖作为一
种年龄信息, 通过调节植株体内miR156的表达而
调控植株对年龄转变的响应(Yang等2013; Yu等
2013)。在年龄途径中, miR156可以抑制SPL的表
达, FUL是SPL蛋白的目标基因。SPL9和SPL10可
以与miR172的启动子特异区域相结合, 从而激活
miR172的转录。因此, miR156通过调控SPL的表达
而间接调控FUL、SOC1、LFY和AP1等MADS-box
基因的表达(Yamaguchi等2005; Wang等2009)。同
时, SPL通过激活miR172而抑制AP3类开花抑制基
因的表达来诱导植株开花。
年龄途径与春化途径存在相互作用。Zhou等
(2013)研究发现, miR156和miR172介导的信号通
路还可以调控RAV基因家族的TOE1基因, 植株在
幼年期, miR156蛋白含量积累, TOE1含量也较高,
此时抑制了植株开花关键基因的转录; 随着植株
进入成年期, miR156含量减少, TOE1的表达也减
弱, 此时持续的适当低温可解除FLC对开花的抑制
作用, 促使植株开花。另外, 年龄途径与GA途径存
在相互交叉, GA信号途径中的DELLA蛋白能与
miR156的靶基因SPL相互作用, DELLA蛋白与SPL
形成的二聚体可以降低SPL的转录活性, 从而使
SPL下游的FUL、SOC1和miR172的表达受到抑制,
从而延迟植株开花(Yu等2012)。
8 成花诱导的整合因子
在拟南芥中, 上述几条成花诱导途径中的基
因效应最终整合于几个重要基因(图1): 春化途径
和自主途径最终汇集于FLC; LFY、SOC1和FT可整
合来自不同成花途径的环境信号, 进而调控花分生
组织转变; 光周期途径和GA途径交汇于LFY, 其启
动子上的顺式作用元件能感应光或GA, 从而激活
FLY的转录表达, LFY既可以调控成花时间, 又能诱
导花分生组织形成(Weigel等1992; Blázquez 1997;
Yu等2012)。光周期途径通过CO来调控FT等基因
的转录水平。FT是光周期途径中CO基因的靶基
因, FT能够与LFY共同诱导AP1的表达而诱导拟南
芥成花。CO不能直接调控SOC1的表达, 而是通过
调控FT的表达而激活SOC1从而促进开花(Yoo等
2005)。在光周期途径突变体中, FT的表达下降, 而
在超量表达CO的转基因植株中, FT的表达又被诱
导表达而表达量升高(Teper-Bamnolker和Samach
2005; Castillejo和Pelaz 2008; Turck等2008)。
9 展望
高等植物中, 成花诱导对成花过程起关键作
用。在不同的季节和地区, 温度和日照长度均有
所不同。有些植物在长期的进化过程中, 逐渐进
化出对不同温度和日照的敏感度, 以便更好地适
应环境。但有些植物对温度和光照要求不严, 可
以在一定环境变化范围内顺利完成生长发育周
期。植物在各种环境条件的综合作用下, 各个成
花诱导途径之间互相交叉和作用, 形成了一些启
动成花的关键基因, 这些基因既相互诱导, 又相互
抑制, 共同作用于植物而使之发生成花转变。各
个成花途径之间即相互独立, 又互相促进, 最终由
FLC、FT等关键基因决定植物成花。目前, 研究
者对这些基因的功能已有一些了解, 而更深入研
究它们的调控网络和作用机制, 可为今后从分子
和生理水平调控植物成花诱导提供背景资料。
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