植物微管骨架参与下胚轴伸长调节机制研究进展

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岳剑茹, 赫云建, 邱天麒, 郭南南, 韩雪萍, 王显玲^,^*沈阳农业大学生物科学技术学院, 沈阳 110866

Research Advances in the Molecular Mechanisms of Plant Microtubules in Regulating Hypocotyl Elongation

Jianru Yue, Yunjian He, Tianqi Qiu, Nannan Guo, Xueping Han, Xianling Wang^,^*College of Bioscience and Biotechnology, Shenyang Agricultural University, Shenyang 110866, China

通讯作者: ^*E-mail:wangxl100@syau.edu.cn

^? 共同第一作者。
责任编辑: 孙冬花
收稿日期:2020-10-13接受日期:2020-12-29网络出版日期:2021-05-01

基金资助:

国家自然科学基金No.31500208
国家自然科学基金No.31970661
辽宁省“兴辽英才计划”青年拔尖人才No.XLYC1807035
沈阳农业大学博士科研启动经费No.880416029

^? These authors contributed equally to this paper
Received:2020-10-13Accepted:2020-12-29Online:2021-05-01

摘要
微管作为细胞骨架的重要成员, 在植物生长发育过程中起重要作用。下胚轴作为研究细胞伸长的模式系统之一, 其伸长受到多种信号的调节。该文综述了微管骨架在响应环境和生长发育信号调节下胚轴伸长过程中的作用及机制, 旨在帮助读者深入理解微管骨架响应上游信号在植物下胚轴伸长中的作用机理。
关键词： 微管;下胚轴;伸长;环境信号;生长发育信号

Abstract
As one of the major members of cytoskeleton, microtubules play important roles in plant growth and deve- lopment. Hypocotyl has become a model system to study cell elongation, which is regulated by multiple internal and ex- ternal signalings. Here, we reviewed the recent research progress for the roles of microtubules in regulating the hypocotyl elongation in response to diversed environmental and developmental cues, which will extend our understanding on how microtubules response to the upstream signal and play roles in the elongation of plant hypocotyls.
Keywords：microtubule;hypocotyl;elongation;environmental signals;growth and developmental cues

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引用本文
岳剑茹, 赫云建, 邱天麒, 郭南南, 韩雪萍, 王显玲. 植物微管骨架参与下胚轴伸长调节机制研究进展. 植物学报, 2021, 56(3): 363-371 doi:10.11983/CBB20170
Yue Jianru, He Yunjian, Qiu Tianqi, Guo Nannan, Han Xueping, Wang Xianling. Research Advances in the Molecular Mechanisms of Plant Microtubules in Regulating Hypocotyl Elongation. Chinese Bulletin of Botany, 2021, 56(3): 363-371 doi:10.11983/CBB20170

植物细胞骨架由微管和微丝组成。微管作为植物细胞骨架成员之一, 在植物生长发育过程中起重要作用(Hashimoto, 2003; Lloyd and Chan, 2004; Hashi- moto and Kato, 2006)。下胚轴作为研究细胞伸长的模式器官, 其伸长既受到许多上游信号的调控也受到微管骨架的调节。早期关于下胚轴伸长的研究中, 细胞骨架和上游信号的调节处于相对独立状态。随着研究的不断深入, 发现微管受到上游信号的调控, 进而参与下胚轴伸长的调节。因此本文对近年来关于微管骨架响应环境和生长发育信号参与下胚轴伸长调节机制的研究进展进行了总结。

1 微管及其功能

微管的基本组成单位是由α-微管蛋白和β-微管蛋白构成的微管蛋白异二聚体, 微管蛋白异二聚体首尾相连并线性排列为1根原纤丝, 13根原纤丝平行排列构成中空的管状结构即为微管。植物细胞中的微管始终处于高度动态状态, 描述微管动态特性的模型有2个: (1) 动态不稳定模型。该模型认为单根微管始终处于动态不稳定状态, 单根微管的两端以一定的“收缩速率”解聚或者以一定的“生长速率”聚合, 整体的微管解聚量和聚合量相对平衡, 因此群体微管处于稳定状态(Mitchison and Kirschner, 1984); (2) 踏车模型。该模型认为单根微管一端不断解聚失去微管蛋白亚基, 另一端则有微管蛋白亚基持续聚合加在其上, 整体表现出单根微管一端不断收缩, 另一端持续生长的踏车现象, 使整根微管保持平衡状态(Margolis and Wilson, 1981)。植物细胞中动态的微管系统在细胞周期中形成4种微管列阵, 分别为间期周质微管列阵、早前期微管带、纺锤体微管列阵和成膜体微管列阵(何群和尤瑞麟, 2004; 李志刚等, 2008)。植物细胞中微管的组织动态均由微管相关蛋白(microtubuleassociated proteins, MAPs)调控。

微管在植物多种生理活动中起重要作用, 如维持细胞形态、控制细胞极性生长、调控细胞有丝分裂与细胞分化以及参与囊泡运输和信号转导(Kost and Chua, 2002; Hashimoto, 2003; Lloyd and Chan, 2004; Hashimoto and Kato, 2006)。4种微管列阵随着细胞周期依次转化, 执行相应的生理功能。其中, 周质微管列阵与植物细胞形态和生长方向等密切相关(Ehrhardt and Shaw, 2006)。在快速伸长的根或黄化下胚轴细胞中, 周质微管表现为密集的横向平行排列(垂直于细胞的伸长方向) (Baskin et al., 2004)。当植物根细胞中的周质微管排列方向由横向变为左手螺旋时, 植物根细胞则转变为右手螺旋方向生长, 即根由向下变为向右生长; 相反, 植物根细胞中的周质微管排列方向由横向变为右手螺旋时, 根细胞则转变为左手螺旋方向生长, 即根由向下变为向左生长(Furutani et al., 2000; Thitamadee et al., 2002; Nakajima et al., 2004)。

2 下胚轴的生长特点

下胚轴是高等植物的胚性器官, 指从子叶着生处以下生出的最初茎的部分。种子在土壤中萌发后, 下胚轴在黑暗条件下快速伸长以破土而出, 使子叶见光生长, 因此下胚轴伸长过程对于植物能否见光生长至关重要。拟南芥(Arabidopsis thaliana)作为模式植物, 其黑暗条件下生长的下胚轴(黄化下胚轴)为研究细胞伸长提供了良好的系统。拟南芥下胚轴由根(下)至子叶(上)一列表皮细胞的数目约为20个。黑暗条件下, 拟南芥下胚轴不同位置的细胞生长速率会随时间发生变化, 即下胚轴细胞的伸长表现出时空梯度特点。种子萌发后, 主要是靠近下胚轴基部的细胞伸长, 在黑暗条件下培养3天后, 靠近基部1-5个细胞的长度占整个下胚轴长度的一半; 继续黑暗培养至4-5天, 下胚轴基部的5个细胞伸长变慢, 中部的6-11个细胞以及上部的9个细胞快速伸长; 黑暗生长6天后, 中部及上部细胞生长速度减慢, 顶端弯钩处细胞伸长; 延长培养时间至7天后, 下胚轴细胞的伸长基本停滞(Gendreau et al., 1997), 表明黄化下胚轴细胞的伸长受时间和空间的精确调控。

3 微管响应环境信号调节下胚轴伸长

植物因固着生长, 其生长发育受到环境因素的影响。下胚轴作为植物体重要的组织器官之一, 其伸长生长受光信号调节。

光是下胚轴伸长的主要调控因子之一。黑暗条件下, 植株下胚轴表现为黄化生长且快速伸长, 见光后下胚轴的伸长速率下降, 说明光对下胚轴伸长有强烈的抑制作用。Le等(2015)研究表明, 在快速伸长的下胚轴细胞内, 周质微管垂直于伸长轴, 表现为横向排列方式, 而在伸长缓慢或停止伸长的下胚轴细胞内, 周质微管表现为斜向或纵向排列; 快速伸长生长的黄化下胚轴见光后, 周质微管由横向平行排列变为斜向或纵向排列, 进而有利于抑制下胚轴的伸长。对光信号调节微管重排的研究发现, 光信号通过改变下胚轴细胞中周质微管的动态及转换能力调控其排列方式, 进而调节下胚轴的伸长。下胚轴细胞在快速伸长之前, 细胞内的微管会形成一种具有双极性的纵向列阵, 并转换为放射状的星状微管列阵, 之后开始进入快速伸长生长。在快速伸长的植株细胞内, 微管的聚合和重排速率都更快(Sambade et al., 2012)。此外, 蓝光可在15分钟内诱导拟南芥下胚轴细胞中横向排列的周质微管完成90度重排。具体机理是: 蓝光照射后微管切割蛋白katanin切割交叉部位的微管产生新末端, 微管正端结合蛋白CLASP (cytoplasmic linker protein-associated protein)稳定新形成的微管末端, 使新末端在伸长过程中改变微管的排列方式为纵向排列(Lindeboom et al., 2013; Wang et al., 2017; Lindeboom et al., 2019) (表1)。该研究结果为揭示光诱导微管重排的分子机理提供了重要线索。

Table 1
表1
表1参与调节下胚轴伸长的微管相关蛋白
Table 1Representative microtubule-associated proteins that are involved in the hypocotyl elongation

蛋白名称	对微管的调节	在下胚轴伸长中的作用	参考文献
Katanin	依赖ATP切割微管	通过蓝光刺激诱导, 在微管交叉部位切断微管, 产生新末端并迅速由横向变为纵向生长, 从而导致下胚轴细胞的生长方向改变	Lindeboom et al., 2013; Wang et al., 2017
CLASP	稳定微管正端	维持下胚轴正常生长, CLASP缺失突变体clasp-1下胚轴明显短于野生型	Ambrose et al., 2007
MDP25	解聚微管	作为下胚轴伸长的负调节因子, MDP25可直接与微管结合, 促进微管解聚, mdp25突变体的黄化下胚轴更长, 而MDP25过表达植株下胚轴较短	Li et al., 2011
WDL3	稳定并重排微管	黑暗下, WDL3被26S蛋白酶体降解, 促进下胚轴伸长; 光调节微管重排过程中, WDL3通过调节下胚轴细胞中微管成束抑制下胚轴伸长	Liu et al., 2013
MDP60	去稳定并重排微管	通过PIF3介导光和乙烯信号, 协同调控微管去稳定蛋白, 促进下胚轴伸长	Ma et al., 2018
SPR1	稳定微管	下胚轴伸长的正向调节因子SPR1在快速生长的下胚轴中高表达, 通过调节微管动态促进黑暗下下胚轴伸长	Nakajima et al., 2004, 2006
WDL5	稳定并重排微管	乙烯激活EIN3, EIN3直接调控WDL5上调表达, WDL5通过维持微管纵向排列抑制黄化下胚轴伸长	Sun et al., 2015
MDP40	去稳定并重排微管	油菜素甾醇激活BZR1, BZR1直接结合到MDP40的启动子上并上调其表达, MDP40解聚微管使其变为横向排列, 从而促进黄化下胚轴伸长	Wang et al., 2012

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此外, 还发现一些参与光信号调节微管重排的微管相关蛋白在下胚轴伸长中起重要作用, 但目前仍不清楚光信号如何调控这些微管相关蛋白。微管去稳定蛋白25 (microtubule destabilizing protein25, MDP 25)在光抑制下胚轴伸长中起重要作用。光信号引起下胚轴细胞中钙离子浓度增加, 使MDP25蛋白从质膜上脱离并进入细胞质, 通过调节周质微管从横向变为斜向或纵向排列, 在下胚轴由黑暗转移至光下后抑制光下下胚轴伸长过程中起重要作用(Li et al., 2011)。Liu等(2013)发现了1个新的在光抑制下胚轴伸长过程中起正调控作用的微管相关蛋白WDL3 (wave-dampened2-like3)。黑暗条件下, WDL3被26S蛋白酶体降解, 无法抑制下胚轴伸长, 而当黄化苗被转移至光下后, WDL3蛋白能稳定表达, 并通过调节下胚轴细胞内周质微管的组织动态抑制下胚轴伸长。Lian等(2017)研究发现, 黑暗条件下, 植物光形态建成的核心调控因子E3泛素连接酶COP1 (constitutive photomorphogenic1)可直接与WDL3结合并使其降解, 该研究揭示了光信号通过直接调控微管相关蛋白水平来调控周质微管重排的新机制。此外, 还有一些微管相关蛋白只特异性地在光下或黑暗下调节下胚轴的伸长。例如, 微管去稳定蛋白MDP60 (microtu bule destabilizing protein60)和微管稳定蛋白SPR1 (SPIRAL1)。MDP60主要在下胚轴表达, 通过改变微管组织和动态来调节下胚轴伸长, 光通过其信号通路的核心转录因子PIF3 (phytochrome-interacting fac-tor 3)负调控MDP60的表达。PIF3作为乙烯促进光下下胚轴伸长的下游关键调节因子, 其蛋白水平受26S蛋白酶体对光信号响应的调节。在光介导的下胚轴伸长过程中, PIF3与MDP60启动子特异性结合, 从而提高MDP60的表达水平, MDP60通过改变微管排列促进下胚轴伸长(Ma et al., 2018)。微管正端结合蛋白SPR1促进黑暗下生长的下胚轴细胞伸长, 在黑暗下生长的下胚轴中可检测到SPR1的表达, 而在光下生长的下胚轴中未检测到SPR1的表达, 表明光影响SPR1表达(Nakajima et al., 2004, 2006; Wang and Mao, 2019)。但尚不清楚响应光调节SPR1表达的上游转录因子, 具体机理有待后续深入研究。

4 微管响应生长发育信号调节下胚轴伸长

植物激素参与调控植物生长发育的各个方面, 下胚轴伸长也受多种激素调控, 如生长素、赤霉素、乙烯和油菜素甾醇, 这些激素处理均可改变下胚轴细胞内微管的排列方式。

4.1 生长素

生长素(auxin)在控制细胞伸长过程中起重要作用。生长素的合成或运输受到影响均会改变拟南芥下胚轴的长度。生长素转运抑制剂NPA (1-naphthylphthala- mic acid)处理和生长素输出载体PIN1 (pin formed1)突变均可抑制光下下胚轴的伸长(Jensen et al., 1998; Friml et al., 2002), 而PIN1过表达可促进光下下胚轴的伸长(De Grauwe et al., 2005)。外源施加生长素或上调生长素合成酶基因的表达都能促进光下生长的拟南芥下胚轴伸长, 黑暗下并无类似作用(Romano et al., 1995; Gray et al., 1998; van der Graaff et al., 2003)。但也有研究表明, 提高生长素的水平会抑制黑暗下下胚轴的伸长。例如, 生长素合成酶基因YUCCA过表达植株, 光下下胚轴比野生型长而黑暗下下胚轴比野生型短, 说明在光暗两种条件下生长素可能发挥不同的作用或通过不同的信号途径发挥作用(Zhao et al., 2001)。

生长素促进下胚轴伸长可通过调节周质微管为横向排列实现。植株体内缺少生长素会抑制其生长, 细胞内的微管以纵向排列为主, 纵向排列的微管可通过外源添加生长素改变为横向排列, 且这种转变具有剂量依赖效应(Fischer and Schopfer, 1997)。关于生长素信号调控微管骨架排列方式分子机制的研究, 从发现生长素能够调节下胚轴细胞内微管的重新排列就已开始。Chen等(2014)研究表明, 生长素通过生长素结合蛋白1 (auxin binding protein 1, ABP1)调节ROP (Rho of plants) GTPase、ROP的互作蛋白RIC1 (ROP-interactive CRIB motif-containing protein 1)和微管切割蛋白katanin来调控下胚轴细胞内的微管骨架重排。True和Shaw (2020)发现, 外源生长素诱导下胚轴细胞周质微管重排需要转运抑制因子/生长素F-box (transport inhibitor 1/auxin F-box, TIR1/AFB)转录途径。但是关于生长素促进下胚轴伸长与调控微管重排之间的关系尚存在不同观点, 有研究者认为, 下胚轴细胞内周质微管重排由生长本身引起, 而不依赖于生长素(Adamowski et al., 2019)。目前, 在生长素调控下胚轴伸长过程中, 并未发现受生长素信号直接调控的微管蛋白或微管相关蛋白, 对于微管骨架响应生长素信号调节下胚轴伸长的机理也需深入研究。

4.2 赤霉素

赤霉素(gibberellin, GA)也参与调控植物下胚轴的伸长(Cowling and Harberd, 1999)。GA可以促进黄瓜(Cucumis sativus)、生菜(Lactuca sativa var. ramosa)和拟南芥等植物下胚轴的伸长。外源添加赤霉素能促进光下生长的拟南芥下胚轴伸长, 但对黑暗下生长的下胚轴无促进效果, 这说明黑暗条件下下胚轴伸长对赤霉素的响应存在饱和效应(Sauret-Güeto et al., 2012)。下胚轴伸长受光和赤霉素的拮抗作用(光抑制细胞伸长, 而赤霉素促进细胞伸长)。具体调节机制为: 在光下, 光受体phyB介导光敏色素互作因子4 (PIF4)降解, PIF4调控的促进下胚轴细胞伸长的下游基因表达受到抑制, 进而抑制下胚轴伸长(Duek and Fankhauser, 2005; de Lucas et al., 2008)。此外, 光使幼苗中赤霉素生物合成基因的表达瞬时下调, 编码赤霉素失活酶基因的表达上调, 因此可能导致活性赤霉素减少及DELLAs (赤霉素信号的负调控因子)蛋白在下胚轴细胞中积累(Peng et al., 1997; Silverstone et al., 1998; Reid et al., 2002; Achard et al., 2007; Alabadíet et al., 2008; Harberd et al., 2009)。DELLA蛋白与促进细胞伸长的转录因子PIF3和PIF4互作抑制其活性, 进而使下胚轴伸长受到抑制。当赤霉素存在时, 赤霉素与受体结合, 促进受体与DELLA蛋白互作, 使DELLAs降解, PIF3和PIF4能发挥其转录活性, 进而促进下胚轴伸长(Feng et al., 2008; de Lucas et al., 2008)。

有研究者对赤霉素促进光下下胚轴伸长过程中微管骨架的功能进行分析, 发现赤霉素通过使下胚轴细胞内周质微管重排为横向进而促进下胚轴伸长(Shibaoka, 1974, 1993)。Vineyard等(2013)使用生长素和赤霉素双激素处理的方法研究了光下生长的下胚轴细胞内横向排列周质微管形成的机制, 发现双激素处理能在2小时内同步诱导光下下胚轴细胞内大部分周质微管变为横向排列。激素处理初期, 正在聚合的微管正端减少约1/3; 继续用激素诱导45分钟后, 横向排列的微管最初在细胞中间部位形成, 然后以双向的方式逐步向细胞顶端和底端扩展(Vineyard et al., 2013)。但也有研究发现, 对光下生长的拟南芥下胚轴外源瞬时施加赤霉素会导致下胚轴细胞的伸长速率瞬时增加, 然后恢复至正常状态, 这一过程伴随DELLAs蛋白中赤霉素合成缺陷突变体抑制子RGA (repressor of ga1-3)蛋白降解及恢复, 但下胚轴表皮细胞外切壁中的周质微管并未变为横向排列, 推测可能光下下胚轴细胞伸长速率的增加并不需要外切壁细胞中周质微管变为横向排列(Sauret-Güeto et al., 2012)。关于微管骨架在赤霉素促进光下下胚轴伸长过程中的作用机制目前仍不十分清楚, 因此, 对微管骨架响应赤霉素信号调节下胚轴伸长的机理也需进一步探索。

4.3 乙烯

乙烯是一种气体激素, 在调控植物下胚轴伸长中起重要作用(Smalle et al., 1997; Zhong et al., 2012)。乙烯可根据光照条件促进或抑制拟南芥下胚轴伸长(Ecker et al.,1995; Smalle et al., 1997)。光照条件下, 乙烯或者其前体ACC (1-aminocyclopropane-1-car-boxylic acid)处理可促进下胚轴伸长; 黑暗条件下, 乙烯则抑制下胚轴伸长(Zhong et al., 2012; Yu et al., 2013)。乙烯通过转录因子EIN3激活PIF3依赖的生长促进途径及乙烯响应因子1 (ethylene response fac-tor 1, ERF1)介导的生长抑制途径来调控下胚轴生长。在光下, 乙烯通过其信号途径关键转录因子EIN3直接结合PIF3的启动子区激活其表达, 从而促进光下下胚轴伸长; 黑暗条件下, 乙烯可诱导抑制伸长的ERF1蛋白积累, 进而抑制黄化下胚轴伸长(Zhong et al., 2012)。此外, 乙烯还可通过COP1介导的HY5 (hypocotyl 5)蛋白降解来促进光下下胚轴的伸长(Yu et al., 2013)。

用外源乙烯或ACC处理时, 黄化下胚轴细胞内周质微管由横向变为纵向排列, 说明乙烯通过调节微管的排列方式参与调节下胚轴的伸长(Soga et al., 2010)。在乙烯调节下胚轴细胞周质微管排列过程中有微管相关蛋白参与。研究表明, 微管相关蛋白WDL5参与乙烯抑制黄化下胚轴伸长的调节(Sun et al., 2015)。黑暗条件下, 乙烯信号通路下游的关键转录因子EIN3直接结合到WDL5的启动子上并上调其表达, WDL5通过稳定并重排微管进而抑制黄化下胚轴的伸长(Sun et al., 2015)。

图1

新窗口打开|下载原图ZIP|生成PPT
图1响应光和激素信号调控下胚轴伸长的微管相关蛋白

COP1: 持续光形态建成1; EIN3/EIL1: 乙烯不敏感3/乙烯不敏感3类似1. CLASP、MDP25、WDL3、MDP60、SPR1、WDL5、MDP40、PIF3、EIN3和BZR1同表1。
Figure 1Microtubule-associated proteins that are involved in hypocotyl elongation and regulated by light and phytohormones

COP1: Constitutive photomorphogenic1; EIN3/EIL1: Ethylene-insensitive 3/EIN3 like 1. CLASP, MDP25, WDL3, MDP60, SPR1, WDL5, MDP40, PIF3, EIN3 and BZR1 see Table 1.

4.4 油菜素甾醇

油菜素甾醇(brassinosteroids, BRs)是一种重要的调节植物生长发育的植物激素(Clouse, 2011; Ye et al., 2011)。BRs通过受体激酶BRI1 (brinsensitive1)以及特定的信号转导途径激活2个关键转录因子BZR1 (brassinazole-resistant 1)和BES1/BZR2 (brinsensi-tive1-EMS-suppressor1/brinsensitive2)来起作用(Li et al., 2010; Kim and Wang, 2010; Clouse, 2011; Gudesblat and Russinova, 2011)。许多油菜素甾醇缺陷及不敏感突变体的黄化下胚轴变短且光下生长的植株矮小。例如, 油菜素甾醇合成缺失突变体det2 (de-etiolated-2)在黑暗下生长时子叶张开且下胚轴伸长受到抑制(Chory et al., 1991; Wang et al., 2001); 油菜素甾醇受体BRI1的无效突变体bri1-116植株也表现出黄化下胚轴短的表型; 油菜素甾醇信号途径转录因子BZR1的激活标签突变体bzr1-1D则表现出黄化下胚轴长且弯曲的表型; 油菜素甾醇信号途径的负调控因子BIN2的显性突变体bin2-1植株黄化下胚轴伸长也受到抑制; 油菜素甾醇信号通路中的上游组分BSKs和BSU1通过改变转录因子BZR1的磷酸化状态调控下胚轴的伸长(Tang et al., 2008; Kim et al., 2010; Gudesblat and Russinova, 2011)。上述结果表明, BRs在调控下胚轴伸长方面起重要作用。

BRs可通过去稳定周质微管改变黄化下胚轴细胞内周质微管由纵向变为横向排列, 进而促进黄化下胚轴的伸长。微管去稳定蛋白参与BRs调控黄化下胚轴细胞中周质微管的重排(Wang et al., 2012)。BRs通过其信号转导途径关键转录因子BZR1结合至编码微管去稳定蛋白MDP40 (microtubule destabilizing protein40)的基因启动子区诱导MDP40表达, MDP- 40通过去稳定周质微管并使其发生重排, 进而促进黄化下胚轴的伸长(Wang et al., 2012)。但在BRs调控植株下胚轴伸长过程中, 微管相关蛋白是瞬时还是持续调节周质微管以及是否有其它微管相关蛋白参与维持动态的周质微管列阵尚不清楚。为更好地理解BRs介导的下胚轴伸长过程中微管及微管相关蛋白的作用, 未来需要通过多种遗传学及生理学实验进行验证。

5 总结与展望

微管骨架是细胞骨架的重要成员之一, 参与多种细胞学过程。下胚轴作为研究植物细胞伸长的模式系统, 微管的组织动态变化会影响下胚轴的伸长。同时, 下胚轴伸长受到多种内部和外部信号调控, 这些信号在调控下胚轴伸长过程中均伴随着周质微管组织排列方式的变化, 但微管骨架响应各种内部及外部信号参与调节下胚轴伸长的机理, 以及微管在信号间互相促进或拮抗调控下胚轴伸长中的作用等问题目前仅进行了初步研究, 还有很多科学问题尚待进一步探索。我们对参与下胚轴伸长调节的微管相关蛋白进行了总结(表1), 并对这些微管蛋白如何响应上游信号参与调节下胚轴伸长进行了归纳(图1)。农业生产上, 种子在土壤中萌发后, 胚轴快速伸长以破土而出, 使子叶见光, 进行光合作用。因此, 阐明微管响应各种内部及外部信号转导途径, 调节下胚轴伸长的机理对于解析下胚轴伸长调节的分子机制和农业生产上提高种子萌发率均具有重要意义。

(责任编辑: 孙冬花)

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(2003). Dynamics and regulation of plant interphase microtubules: a comparative view
Curr Opin Plant Biol 6, 568-576.

PMID:14611955 [本文引用: 1]

Microtubule and actin cytoskeletons are fundamental to a variety of cellular activities within eukaryotic organisms. Extensive information on the dynamics and functions of microtubules, as well as on their regulatory proteins, have been revealed in fungi and animals, and corresponding pictures are now slowly emerging in plants. During interphase, plant cells contain highly dynamic cortical microtubules that organize into ordered arrays, which are apparently regulated by distinct groups of microtubule regulators. Comparison with fungal and animal microtubules highlights both conserved and unique mechanisms for the regulation of the microtubule cytoskeleton in plants.

[27]

Hashimoto

, Kato

(2006). Cortical control of plant microtubules
Curr Opin Plant Biol 9, 5-11.

PMID:16324879 [本文引用: 2]

The cortical microtubule array of plant cells appears in early G(1) and remodels during the progression of the cell cycle and differentiation, and in response to various stimuli. Recent studies suggest that cortical microtubules are mostly formed on pre-existing microtubules and, after detachment from the initial nucleation sites, actively interact with each other to attain distinct distribution patterns. The plus end of growing microtubules is thought to accumulate protein complexes that regulate both microtubule dynamics and interactions with cortical targets. The ROP family of small GTPases and the mitogen-activated protein kinase pathways have emerged as key players that mediate the cortical control of plant microtubules.

[28]

Jensen

, Hangarter

, Estelle

(1998). Auxin transport is required for hypocotyl elongation in light-grown but not dark-grownArabidopsis
Plant Physiol 116, 455-462.

PMID:9489005 [本文引用: 1]

Many auxin responses are dependent on redistribution and/or polar transport of indoleacetic acid. Polar transport of auxin can be inhibited through the application of phytotropins such as 1-naphthylphthalamic acid (NPA). When Arabidopsis thaliana seedlings were grown in the light on medium containing 1.0 microM NPA, hypocotyl and root elongation and gravitropism were strongly inhibited. When grown in darkness, however, NPA disrupted the gravity response but did not affect elongation. The extent of inhibition of hypocotyl elongation by NPA increased in a fluence-rate-dependent manner to a maximum of about 75% inhibition at 50 mumol m-2 s-1 of white light. Plants grown under continuous blue or far-red light showed NPA-induced hypocotyl inhibition similar to that of white-light-grown plants. Plants grown under continuous red light showed less NPA-induced inhibition. Analysis of photoreceptor mutants indicates the involvement of phytochrome and cryptochrome in mediating this NPA response. Hypocotyls of some auxin-resistant mutants had decreased sensitivity to NPA in the light, but etiolated seedlings of these mutants were similar in length to the wild type. These results indicate that light has a significant effect on NPA-induced inhibition in Arabidopsis, and suggest that auxin has a more important role in elongation responses in light-grown than in dark-grown seedlings.

[29]

Kim

, Kim

, Lim

, Nam

(2010). Constitutive activation of stress-inducible genes in a brassinosteroid-insensitive 1(bri1) mutant results in higher tolerance to cold
Physiol Plant 138, 191-204.

[本文引用: 1]

[30]

Kim

, Wang

(2010). Brassinosteroid signal transduc-tion from receptor kinases to transcription factors
Annu Rev Plant Biol 61, 681-704.

DOI:10.1146/annurev.arplant.043008.092057 URL [本文引用: 1]

[31]

Kost

, Chua

(2002). The plant cytoskeleton: vacuoles and cell walls make the difference
Cell 108, 9-12.

DOI:10.1016/S0092-8674(01)00634-1 URL

[32]

, Vandenbussche

, de Cnodder

, van der Straeten

, Verbelen

(2005). Cell elongation and microtubule behavior in the Arabidopsis hypocotyl: responses to ethy- lene and auxin
J Plant Growth Regul 24, 166-178.

DOI:10.1007/s00344-005-0044-8 URL [本文引用: 3]

[33]

, Wang

, Qin

, Zhang

, Liu

, Sun

, Zhou

, Zhu

, Zhang

, Yuan

, Mao

(2011). MDP25, a novel calcium regulatory protein, mediates hypocotyl cell elongation by destabilizing cortical microtubules in Ara- bidopsis
Plant Cell 23, 4411-4427.

DOI:10.1105/tpc.111.092684 URL [本文引用: 2]

[34]

, Ye

, Guo

, Yin

(2010). Arabidopsis IWS1 interacts with transcription factor BES1 and is involved in plant steroid hormone brassinosteroid regulated gene expression
Proc Natl Acad Sci USA 107, 3918-3923.

DOI:10.1073/pnas.0909198107 URL

[35]

Lian

, Liu

, Wang

, Zhou

, Li

, Mao

(2017). COP1 mediates dark-specific degradation of micro- tubule-associated protein WDL3 in regulating Arabidopsis hypocotyl elongation
Proc Natl Acad Sci USA 114, 12321-12326.

DOI:10.1073/pnas.1708087114 URL [本文引用: 2]

[36]

Lindeboom

, Nakamura

, Hibbel

, Shundyak

, Gutierrez

, Ketelaar

, Emons

AMC

, Mulder

, Kirik

, Ehrhardt

(2013). A mechanism for reorientation of cortical microtubule arrays driven by microtubule seve- ring
Science 342, 1245533.

DOI:10.1126/science.1245533 URL [本文引用: 2]

[37]

Lindeboom

, Nakamura

, Saltini

, Hibbel

, Walia

, Ketelaar

, Emons

AMC

, Sedbrook

, Kirik

, Mulder

, Ehrhardt

(2019). CLASP stabilization of plus ends created by severing promotes microtubule creation and reorientation
J Cell Biol 218, 190-205.

DOI:10.1083/jcb.201805047

Central to the building and reorganizing cytoskeletal arrays is creation of new polymers. Although nucleation has been the major focus of study for microtubule generation, severing has been proposed as an alternative mechanism to create new polymers, a mechanism recently shown to drive the reorientation of cortical arrays of higher plants in response to blue light perception. Severing produces new plus ends behind the stabilizing GTP-cap. An important and unanswered question is how these ends are stabilized in vivo to promote net microtubule generation. Here we identify the conserved protein CLASP as a potent stabilizer of new plus ends created by katanin severing in plant cells. Clasp mutants are defective in cortical array reorientation. In these mutants, both rescue of shrinking plus ends and the stabilization of plus ends immediately after severing are reduced. Computational modeling reveals that it is the specific stabilization of severed ends that best explains CLASP's function in promoting microtubule amplification by severing and array reorientation.

[38]

Liu

, Qin

, Ma

, Sun

, Liu

, Yuan

, Mao

(2013). Light-regulated hypocotyl elongation involves proteasome-dependent degradation of the microtubule regulatory protein WDL3 in Arabidopsis
Plant Cell 25, 1740-1755.

DOI:10.1105/tpc.113.112789 URL [本文引用: 3]

[39]

Lloyd

, Chan

(2004). Microtubules and the shape of plants to come
Nat Rev Mol Cell Biol 5, 13-23.

[本文引用: 1]

[40]

, Wang

, Sun

, Mao

(2018). Coordinated regulation of hypocotyl cell elongation by light and ethy- lene through a microtubule destabilizing protein
Plant Phy- siol 176, 678-690.

[本文引用: 2]

[41]

Margolis

, Wilson

(1981). Microtubule treadmills— possible molecular machinery
Nature 293, 705-711.

PMID:7027052 [本文引用: 1]

Microtubule polymerization in vitro is the summation of different reactions occurring at each end of the polymer. In steady-state conditions in vitro, net tubulin addition on the microtubule occurs at one end of the polymer, and net tubulin loss occurs at the opposite end. Thus, a unidirectional flux of tubulin from one end of the microtubule to the other, or "treadmilling', can occur. The opposite end assembly--disassembly behaviour of microtubules, if it occurs within cells, could be fundamentally linked to the functions of microtubules, as, for example, in the translocation of chromosomes during mitosis.

[42]

Mitchison

, Kirschner

(1984). Dynamic instability of microtubule growth
Nature 312, 237-242.

PMID:6504138 [本文引用: 2]

We report here that microtubules in vitro coexist in growing and shrinking populations which interconvert rather infrequently. This dynamic instability is a general property of microtubules and may be fundamental in explaining cellular microtubule organization.

[43]

Nakajima

, Furutani

, Tachimoto

, Matsubara

, Hashimoto

(2004). SPIRAL1 encodes a plant-specific microtubule-localized protein required for directional control of rapidly expanding Arabidopsis cells
Plant Cell 16, 1178-1190.

PMID:15084720 [本文引用: 2]

Highly organized interphase cortical microtubule (MT) arrays are essential for anisotropic growth of plant cells, yet little is known about the molecular mechanisms that establish and maintain the order of these arrays. The Arabidopsis thaliana spiral1 (spr1) mutant shows right-handed helical growth in roots and etiolated hypocotyls. Characterization of the mutant phenotypes suggested that SPR1 may control anisotropic cell expansion through MT-dependent processes. SPR1 was identified by map-based cloning and found to encode a small protein with unknown function. Proteins homologous to SPR1 occur specifically and ubiquitously in plants. Genetic complementation with green fluorescent protein fusion proteins indicated that the SPR1 protein colocalizes with cortical MTs and that both MT localization and cell expansion control are conferred by the conserved N- and C-terminal regions. Strong SPR1 expression was found in tissues undergoing rapid cell elongation. Plants overexpressing SPR1 showed enhanced resistance to an MT drug and increased hypocotyl elongation. These observations suggest that SPR1 is a plant-specific MT-localized protein required for the maintenance of growth anisotropy in rapidly elongating cells.

[44]

Nakajima

, Kawamura

, Hashimoto

(2006). Role of the SPIRAL1 gene family in anisotropic growth of Arabi-dopsis thaliana
Plant Cell Physiol 47, 513-522.

PMID:16478750 [本文引用: 2]

Arabidopsis spiral1 (spr1) mutants show a right-handed helical growth phenotype in roots and etiolated hypocotyls due to impaired directional growth of rapidly expanding cells. SPR1 encodes a small protein with as yet unknown biochemical functions, though its localization to cortical microtubules (MTs) suggests that SPR1 maintains directional cell expansion by regulating cortical MT functions. The Arabidopsis genome contains five SPR1-LIKE (SP1L) genes that share high sequence identity in N- and C-terminal regions. Overexpression of SP1Ls rescued the helical growth phenotype of spr1, indicating that SPR1 and SP1L proteins share the same biochemical functions. Expression analyses revealed that SPR1 and SP1L genes are transcribed in partially overlapping tissues. A combination of spr1 and sp1l mutations resulted in randomly oriented cortical MT arrays and isotropic expansion of epidermal cells. These observations suggest that SPR1 and SP1Ls act redundantly in maintaining the cortical MT organization essential for anisotropic cell growth, and that the helical growth phenotype of spr1 results from a partially compromised state of cortical MTs. Additionally, inflorescence stems of spr1 sp1l multiple mutants showed a right-handed tendril-like twining growth, indicating that a directional winding response may be conferred to the non-directional nutational movement by modulating the expression of SPR1 homologs.

[45]

Peng

, Carol

, Richards

, King

, Cowling

, Murphy

, Harberd

(1997). The Arabidopsis GAI gene defines a signaling pathway that negatively regulates gibberellin responses
Genes Dev 11, 3194-3205.

DOI:10.1101/gad.11.23.3194 URL [本文引用: 1]

[46]

Reid

, Botwright

, Smith

, O’Neill

, Kerckhoffs

LHJ

(2002). Control of gibberellin levels and gene expres- sion during de-etiolation in pea
Plant Physiol 128, 734-741.

DOI:10.1104/pp.010607 URL [本文引用: 1]

[47]

Romano

, Robson

PRH

, Smith

, Estelle

, Klee

(1995). Transgene-mediated auxin overproduction in Ara- bidopsis: hypocotyl elongation phenotype and interactions with the hy6-1 hypocotyl elongation and axr1 auxin-resis tant mutants
Plant Mol Biol 27, 1071-1083.

PMID:7766890 [本文引用: 1]

Transgenic Arabidopsis thaliana plants constitutively expressing Agrobacterium tumefaciens tryptophan monooxygenase (iaaM) were obtained and characterized. Arabidopsis plants expressing iaaM have up to 4-fold higher levels of free indole-3-acetic acid (IAA) and display increased hypocotyl elongation in the light. This result clearly demonstrates that excess endogenous auxin can promote cell elongation in a whole plant. Interactions of the auxin-overproducing transgenic plants with the phytochrome-deficient hy6-1 and auxin-resistant axr1-3 mutations were also studied. The effects of auxin overproduction on hypocotyl elongation were not additive to the effects of phytochrome deficiency in the hy6-1 mutant, indicating that excess auxin does not counteract factors that limit hypocotyl elongation in hy6-1 seedlings. Auxin-overproducing seedlings are also qualitatively indistinguishable from wild-type controls in their response to red, far-red, and blue light treatments, demonstrating that the effect of excess auxin on hypocotyl elongation is independent of red and blue light-mediated effects. All phenotypic effects of iaaM-mediated auxin overproduction (i.e. increased hypocotyl elongation in the light, severe rosette leaf epinasty, and increased apical dominance) are suppressed by the auxin-resistant axr1-3 mutation. The axr1-3 mutation apparently blocks auxin signal transduction since it does not reduce auxin levels when combined with the auxin-overproducing transgene.

[48]

Sambade

, Pratap

, Buschmann

, Morris

, Lloyd

(2012). The influence of light on microtubule dynamics and alignment in the Arabidopsis hypocotyl
Plant Cell 24, 192-201.

DOI:10.1105/tpc.111.093849 URL [本文引用: 2]

[49]

Sauret-Güeto

, Calder

, Harberd

(2012). Transient gibberellin application promotes Arabidopsis thaliana hypocotyl cell elongation without maintaining transverse o- rientation of microtubules on the outer tangential wall of epidermal cells
Plant J 69, 628-639.

DOI:10.1111/tpj.2012.69.issue-4 URL [本文引用: 1]

[50]

Shibaoka

(1974). Involvement of wall microtubules in gibberellin promotion and kinetin inhibition of stem elongation
Plant Cell Physiol 15, 255-263.

[本文引用: 1]

[51]

Shibaoka

(1993). Regulation by gibberellins of the orientation of cortical microtubules in plant cells
Aust J Plant Physiol 20, 461-470.

[本文引用: 1]

[52]

Silverstone

, Ciampaglio

, Sun

(1998). The Arabidopsis RGA gene encodes a transcriptional regulator repressing the gibberellin signal transduction pathway
Plant Cell 10, 155-169.

PMID:9490740 [本文引用: 2]

The recessive rga mutation is able to partially suppress phenotypic defects of the Arabidopsis gibberellin (GA) biosynthetic mutant ga1-3. Defects in stem elongation, flowering time, and leaf abaxial trichome initiation are suppressed by rga. This indicates that RGA is a negative regulator of the GA signal transduction pathway. We have identified 10 additional alleles of rga from a fast-neutron mutagenized ga1-3 population and used them to isolate the RGA gene by genomic subtraction. Our data suggest that RGA may be functioning as a transcriptional regulator. RGA was found to be a member of the VHIID regulatory family, which includes the radial root organizing gene SCARECROW and another GA signal transduction repressor, GAI. RGA and GAI proteins share a high degree of homology, but their N termini are more divergent. The presence of several structural features, including homopolymeric serine and threonine residues, a putative nuclear localization signal, leucine heptad repeats, and an LXXLL motif, indicates that the RGA protein may be a transcriptional regulator that represses the GA response. In support of the putative nuclear localization signal, we demonstrated that a transiently expressed green fluorescent protein-RGA fusion protein is localized to the nucleus in onion epidermal cells. Because the rga mutation abolished the high level of expression of the GA biosynthetic gene GA4 in the ga1-3 mutant background, we conclude that RGA may also play a role in controlling GA biosynthesis.

[53]

Smalle

, Haegman

, Kurepa

, van Montagu

, Straeten

DVD

(1997). Ethylene can stimulate Arabidopsis hypocotyl elongation in the light
Proc Natl Acad Sci USA 94, 2756-2761.

DOI:10.1073/pnas.94.6.2756 URL [本文引用: 1]

[54]

Soga

, Yamaguchi

, Kotake

, Wakabayashi

, Hoson

(2010). Transient increase in the levels of γ-tubulin complex and katanin are responsible for reorientation by ethylene and hypergravity of cortical microtubules
Plant Signal Behav 5, 1480-1482.

DOI:10.4161/psb.5.11.13561 URL [本文引用: 2]

[55]

Sun

, Ma

, Mao

(2015). Ethylene regulates the Arabidopsis microtubule-associated protein WAVE-DAM- PENED2-LIKE5 in etiolated hypocotyl elongation
Plant Physiol 169, 325-337.

[本文引用: 2]

[56]

Tang

, Kim

, Oses-Prieto

, Sun

, Deng

, Zhu

, Wang

, Burlingame

, Wang

(2008). BSKs mediate signal transduction from the receptor kinase BRI1 in Arabidopsis
Science 321, 557-560.

DOI:10.1126/science.1156973 URL [本文引用: 1]

[57]

Thitamadee

, Tuchihara

, Hashimoto

(2002). Microtubule basis for left-handed helical growth inArabidopsis
Nature 417, 193-196.

PMID:12000963

Left-right asymmetry in plants can be found in helices of stalks, stems and tendrils, and in fan-like petal arrangements. The handedness in these asymmetric structures is often fixed in given species, indicating that genetic factors control asymmetric development. Here we show that dominant negative mutations at the tubulin intradimer interface of alpha-tubulins 4 and 6 cause left-handed helical growth and clockwise twisting in elongating organs of Arabidopsis thaliana. We demonstrate that the mutant tubulins incorporate into microtubule polymers, producing right-handed obliquely oriented cortical arrays, in the root epidermal cells. The cortical microtubules in the mutants had increased sensitivity to microtubule-specific drugs. These results suggest that reduced microtubule stability can produce left-handed helical growth in plants.

[58]

True

, Shaw

(2020). Exogenous auxin induces trans- verse microtubule arrays through TRANSPORT INHIBI-TOR RESPONSE1/AUXIN SIGNALING F-BOX receptors
Plant Physiol 182, 892-907.

DOI:10.1104/pp.19.00928 URL [本文引用: 2]

[59]

van der Graaff

, Nussbaumer

, Keller

(2003). The Arabidopsis thaliana rlp mutations revert the ectopic leaf blade formation conferred by activation tagging of the LEP gene
Mol Genet Genomics 270, 243-252.

PMID:12910411 [本文引用: 1]

Activation tagging of the gene LEAFY PETIOLE (LEP) with a T-DNA construct induces ectopic leaf blade formation in Arabidopsis, which results in a leafy petiole phenotype. In addition, the number of rosette leaves produced prior to the onset of bolting is reduced, and the rate of leaf initiation is retarded by the activation tagged LEP gene. The ectopic leaf blade results from an invasion of the petiole region by the wild-type leaf blade. In order to isolate mutants that are specifically disturbed in the outgrowth of the leaf blade, second site mutagenesis was performed using ethane methanesulphonate (EMS) on a transgenic line that harbours the activation-tagged LEP gene and exhibits the leafy petiole phenotype. A collection of revertant for leafy petiole (rlp lines was isolated that form petiolated rosette leaves in the presence of the activated LEP gene, and could be classified into three groups. The class III rlp lines also display altered leaf development in a wild-type (non-transgenic) background, and are probably mutated in genes that affect shoot or leaf development. The rlp lines of classes I and II, which represent the majority of revertants, do not affect leaf blade outgrowth in a wild-type (non-transgenic) background. This indicates that LEP regulates a subset of the genes involved in the process of leaf blade outgrowth, and that genetic and/or functional redundancy in this process compensates for the loss of RLP function during the formation of the wild-type leaf blade. More detailed genetic and morphological analyses were performed on a selection of the rlp lines. Of these, the dominant rlp lines display complete reversion of (1) the leafy petiole phenotype, (2) the reduction in the number of rosette leaves and (3) the slower leaf initiation rate caused by the activation-tagged LEP gene. Therefore, these lines are potentially mutated in genes for interacting partners of LEP or in downstream regulatory genes. In contrast, the recessive rlp lines exhibit a specific reversion of the leafy petiole phenotype. Thus, these lines are most probably mutated in genes specific for the outgrowth of the leaf blade. Further functional analysis of the rlp mutations will contribute to the dissection of the complex pathways underlying leaf blade outgrowth.

[60]

Vineyard

, Elliott

, Dhingra

, Lucas

, Shaw

(2013). Progressive transverse microtubule array organization in hormone-induced Arabidopsis hypocotyl cells
Plant Cell 25, 662-676.

[本文引用: 2]

[61]

Wang

, Liu

, Wang

, Li

, Dong

, Han

, Wang

, Tian

, Yu

, Gao

, Kong

(2017). KTN80 confers precision to microtubule severing by specific targeting of Katanin complexes in plant cells
EMBO J 36, 3435-3447.

DOI:10.15252/embj.201796823 URL [本文引用: 2]

[62]

Wang

, Mao

(2019). Understanding the functions and mechanisms of plant cytoskeleton in response to environmental signals
Curr Opin Plant Biol 52, 86-96.

DOI:10.1016/j.pbi.2019.08.002 URL [本文引用: 2]

[63]

Wang

, Zhang

, Yuan

, Ehrhardt

, Wang

, Mao

(2012). Arabidopsis microtubule destabilizing protein40 is involved in brassinosteroid regulation of hypocotyl elongation
Plant Cell 24, 4012-4025.

DOI:10.1105/tpc.112.103838 URL [本文引用: 2]

[64]

Wang

, Seto

, Fujioka

, Yoshida

, Chory

(2001). BRI1 is a critical component of a plasma-membrane receptor for plant steroids
Nature 410, 380-383.

PMID:11268216 [本文引用: 1]

Most multicellular organisms use steroids as signalling molecules for physiological and developmental regulation. Two different modes of steroid action have been described in animal systems: the well-studied gene regulation response mediated by nuclear receptors, and the rapid non-genomic responses mediated by proposed membrane-bound receptors. Plant genomes do not seem to encode members of the nuclear receptor superfamily. However, a transmembrane receptor kinase, brassinosteroid-insensitive1 (BRI1), has been implicated in brassinosteroid responses. Here we show that BRI1 functions as a receptor of brassinolide, the most active brassinosteroid. The number of brassinolide-binding sites and the degree of response to brassinolide depend on the level of BRI1 protein. The brassinolide-binding activity co-immunoprecipitates with BRI1, and requires a functional BRI1 extracellular domain. Moreover, treatment of Arabidopsis seedlings with brassinolide induces autophosphorylation of BRI1, which, together with our binding studies, shows that BRI1 is a receptor kinase that transduces steroid signals across the plasma membrane.

[65]

, Li

, Yin

(2011). Recent advances in the regulation of brassinosteroid signaling and biosynthesis pathways
J Integr Plant Biol 53, 455-468.

DOI:10.1111/jipb.2011.53.issue-6 URL [本文引用: 2]

[66]

, Wang

, Zhang

, Quan

, Zhang

, Deng

, Ma

, Huang

(2013). Ethylene promotes hypocotyl growth and HY5 degradation by enhancing the movement of COP1 to the nucleus in the light
PLoS Ge- net 9, e1004025.

[本文引用: 1]

[67]

Zhao

, Christensen

, Fankhauser

, Cashman

, Cohen

, Weigel

, Chory

(2001). A role for flavin monooxygenase-like enzymes in auxin biosynthesis
Science 291, 306-309.

DOI:10.1126/science.291.5502.306 URL [本文引用: 3]

[68]

Zhong

, Shi

, Xue

, Wang

, Xi

, Li

, Quail

, Deng

, Guo

(2012). A molecular framework of light-controlled phytohormone action in Arabidopsis
Curr Biol 22, 1530-1535.

DOI:10.1016/j.cub.2012.06.039 URL

应用Steedman’s wax切片法观察植物细胞微管骨架
1
2004

... 微管的基本组成单位是由α-微管蛋白和β-微管蛋白构成的微管蛋白异二聚体, 微管蛋白异二聚体首尾相连并线性排列为1根原纤丝, 13根原纤丝平行排列构成中空的管状结构即为微管.植物细胞中的微管始终处于高度动态状态, 描述微管动态特性的模型有2个: (1) 动态不稳定模型.该模型认为单根微管始终处于动态不稳定状态, 单根微管的两端以一定的“收缩速率”解聚或者以一定的“生长速率”聚合, 整体的微管解聚量和聚合量相对平衡, 因此群体微管处于稳定状态(Mitchison and Kirschner, 1984); (2) 踏车模型.该模型认为单根微管一端不断解聚失去微管蛋白亚基, 另一端则有微管蛋白亚基持续聚合加在其上, 整体表现出单根微管一端不断收缩, 另一端持续生长的踏车现象, 使整根微管保持平衡状态(Margolis and Wilson, 1981).植物细胞中动态的微管系统在细胞周期中形成4种微管列阵, 分别为间期周质微管列阵、早前期微管带、纺锤体微管列阵和成膜体微管列阵(何群和尤瑞麟, 2004; 李志刚等, 2008).植物细胞中微管的组织动态均由微管相关蛋白(microtubuleassociated proteins, MAPs)调控. ...

甘蔗茎尖细胞有丝分裂过程中微管骨架的变化
1
2008

... 微管的基本组成单位是由α-微管蛋白和β-微管蛋白构成的微管蛋白异二聚体, 微管蛋白异二聚体首尾相连并线性排列为1根原纤丝, 13根原纤丝平行排列构成中空的管状结构即为微管.植物细胞中的微管始终处于高度动态状态, 描述微管动态特性的模型有2个: (1) 动态不稳定模型.该模型认为单根微管始终处于动态不稳定状态, 单根微管的两端以一定的“收缩速率”解聚或者以一定的“生长速率”聚合, 整体的微管解聚量和聚合量相对平衡, 因此群体微管处于稳定状态(Mitchison and Kirschner, 1984); (2) 踏车模型.该模型认为单根微管一端不断解聚失去微管蛋白亚基, 另一端则有微管蛋白亚基持续聚合加在其上, 整体表现出单根微管一端不断收缩, 另一端持续生长的踏车现象, 使整根微管保持平衡状态(Margolis and Wilson, 1981).植物细胞中动态的微管系统在细胞周期中形成4种微管列阵, 分别为间期周质微管列阵、早前期微管带、纺锤体微管列阵和成膜体微管列阵(何群和尤瑞麟, 2004; 李志刚等, 2008).植物细胞中微管的组织动态均由微管相关蛋白(microtubuleassociated proteins, MAPs)调控. ...

DELLAs contribute to plant photomorphogenesis
1
2007

... 赤霉素(gibberellin, GA)也参与调控植物下胚轴的伸长(Cowling and Harberd, 1999).GA可以促进黄瓜(Cucumis sativus)、生菜(Lactuca sativa var. ramosa)和拟南芥等植物下胚轴的伸长.外源添加赤霉素能促进光下生长的拟南芥下胚轴伸长, 但对黑暗下生长的下胚轴无促进效果, 这说明黑暗条件下下胚轴伸长对赤霉素的响应存在饱和效应(Sauret-Güeto et al., 2012).下胚轴伸长受光和赤霉素的拮抗作用(光抑制细胞伸长, 而赤霉素促进细胞伸长).具体调节机制为: 在光下, 光受体phyB介导光敏色素互作因子4 (PIF4)降解, PIF4调控的促进下胚轴细胞伸长的下游基因表达受到抑制, 进而抑制下胚轴伸长(Duek and Fankhauser, 2005; de Lucas et al., 2008).此外, 光使幼苗中赤霉素生物合成基因的表达瞬时下调, 编码赤霉素失活酶基因的表达上调, 因此可能导致活性赤霉素减少及DELLAs (赤霉素信号的负调控因子)蛋白在下胚轴细胞中积累(Peng et al., 1997; Silverstone et al., 1998; Reid et al., 2002; Achard et al., 2007; Alabadíet et al., 2008; Harberd et al., 2009).DELLA蛋白与促进细胞伸长的转录因子PIF3和PIF4互作抑制其活性, 进而使下胚轴伸长受到抑制.当赤霉素存在时, 赤霉素与受体结合, 促进受体与DELLA蛋白互作, 使DELLAs降解, PIF3和PIF4能发挥其转录活性, 进而促进下胚轴伸长(Feng et al., 2008; de Lucas et al., 2008). ...

Reorientation of cortical microtubule arrays in the hypocotyl of Arabidopsis thaliana is induced by the cell growth process and independent of auxin signaling
1
2019

... 生长素促进下胚轴伸长可通过调节周质微管为横向排列实现.植株体内缺少生长素会抑制其生长, 细胞内的微管以纵向排列为主, 纵向排列的微管可通过外源添加生长素改变为横向排列, 且这种转变具有剂量依赖效应(Fischer and Schopfer, 1997).关于生长素信号调控微管骨架排列方式分子机制的研究, 从发现生长素能够调节下胚轴细胞内微管的重新排列就已开始.Chen等(2014)研究表明, 生长素通过生长素结合蛋白1 (auxin binding protein 1, ABP1)调节ROP (Rho of plants) GTPase、ROP的互作蛋白RIC1 (ROP-interactive CRIB motif-containing protein 1)和微管切割蛋白katanin来调控下胚轴细胞内的微管骨架重排.True和Shaw (2020)发现, 外源生长素诱导下胚轴细胞周质微管重排需要转运抑制因子/生长素F-box (transport inhibitor 1/auxin F-box, TIR1/AFB)转录途径.但是关于生长素促进下胚轴伸长与调控微管重排之间的关系尚存在不同观点, 有研究者认为, 下胚轴细胞内周质微管重排由生长本身引起, 而不依赖于生长素(Adamowski et al., 2019).目前, 在生长素调控下胚轴伸长过程中, 并未发现受生长素信号直接调控的微管蛋白或微管相关蛋白, 对于微管骨架响应生长素信号调节下胚轴伸长的机理也需深入研究. ...

Gibberellins modulate light signaling pathways to prevent Arabidopsis seedling de-etiolation in darkness
1
2008

... 赤霉素(gibberellin, GA)也参与调控植物下胚轴的伸长(Cowling and Harberd, 1999).GA可以促进黄瓜(Cucumis sativus)、生菜(Lactuca sativa var. ramosa)和拟南芥等植物下胚轴的伸长.外源添加赤霉素能促进光下生长的拟南芥下胚轴伸长, 但对黑暗下生长的下胚轴无促进效果, 这说明黑暗条件下下胚轴伸长对赤霉素的响应存在饱和效应(Sauret-Güeto et al., 2012).下胚轴伸长受光和赤霉素的拮抗作用(光抑制细胞伸长, 而赤霉素促进细胞伸长).具体调节机制为: 在光下, 光受体phyB介导光敏色素互作因子4 (PIF4)降解, PIF4调控的促进下胚轴细胞伸长的下游基因表达受到抑制, 进而抑制下胚轴伸长(Duek and Fankhauser, 2005; de Lucas et al., 2008).此外, 光使幼苗中赤霉素生物合成基因的表达瞬时下调, 编码赤霉素失活酶基因的表达上调, 因此可能导致活性赤霉素减少及DELLAs (赤霉素信号的负调控因子)蛋白在下胚轴细胞中积累(Peng et al., 1997; Silverstone et al., 1998; Reid et al., 2002; Achard et al., 2007; Alabadíet et al., 2008; Harberd et al., 2009).DELLA蛋白与促进细胞伸长的转录因子PIF3和PIF4互作抑制其活性, 进而使下胚轴伸长受到抑制.当赤霉素存在时, 赤霉素与受体结合, 促进受体与DELLA蛋白互作, 使DELLAs降解, PIF3和PIF4能发挥其转录活性, 进而促进下胚轴伸长(Feng et al., 2008; de Lucas et al., 2008). ...

The Arabidopsis CLASP gene encodes a microtubule-associated protein involved in cell expansion and division
1
2007

... Representative microtubule-associated proteins that are involved in the hypocotyl elongation

Table 1

蛋白名称	对微管的调节	在下胚轴伸长中的作用	参考文献
Katanin	依赖ATP切割微管	通过蓝光刺激诱导, 在微管交叉部位切断微管, 产生新末端并迅速由横向变为纵向生长, 从而导致下胚轴细胞的生长方向改变	Lindeboom et al., 2013; Wang et al., 2017
CLASP	稳定微管正端	维持下胚轴正常生长, CLASP缺失突变体clasp-1下胚轴明显短于野生型	Ambrose et al., 2007
MDP25	解聚微管	作为下胚轴伸长的负调节因子, MDP25可直接与微管结合, 促进微管解聚, mdp25突变体的黄化下胚轴更长, 而MDP25过表达植株下胚轴较短	Li et al., 2011
WDL3	稳定并重排微管	黑暗下, WDL3被26S蛋白酶体降解, 促进下胚轴伸长; 光调节微管重排过程中, WDL3通过调节下胚轴细胞中微管成束抑制下胚轴伸长	Liu et al., 2013
MDP60	去稳定并重排微管	通过PIF3介导光和乙烯信号, 协同调控微管去稳定蛋白, 促进下胚轴伸长	Ma et al., 2018
SPR1	稳定微管	下胚轴伸长的正向调节因子SPR1在快速生长的下胚轴中高表达, 通过调节微管动态促进黑暗下下胚轴伸长	Nakajima et al., 2004, 2006
WDL5	稳定并重排微管	乙烯激活EIN3, EIN3直接调控WDL5上调表达, WDL5通过维持微管纵向排列抑制黄化下胚轴伸长	Sun et al., 2015
MDP40	去稳定并重排微管	油菜素甾醇激活BZR1, BZR1直接结合到MDP40的启动子上并上调其表达, MDP40解聚微管使其变为横向排列, 从而促进黄化下胚轴伸长	Wang et al., 2012

CLASP: Cytoplasmic linker protein-associated protein; MDP25: Microtubule destabilizing protein 25; WDL3: Wave-dampened 2 like 3; MDP60: Microtubule destabilizing protein 60; SPR1: Spiral 1; WDL5: Wave-dampened 2 like 5; MDP40: Microtubule destabilizing protein 40; PIF3: Phytochrome-interacting factor 3; EIN3: Ethylene-insensitive 3; BZR1: Brassinazole-resistant 1 ...

Disorganization of cortical microtubules stimulates tangential expansion and reduces the uniformity of cellulose microfibril alignment among cells in the root of Ara- bidopsis
1
2004

... 微管在植物多种生理活动中起重要作用, 如维持细胞形态、控制细胞极性生长、调控细胞有丝分裂与细胞分化以及参与囊泡运输和信号转导(Kost and Chua, 2002; Hashimoto, 2003; Lloyd and Chan, 2004; Hashimoto and Kato, 2006).4种微管列阵随着细胞周期依次转化, 执行相应的生理功能.其中, 周质微管列阵与植物细胞形态和生长方向等密切相关(Ehrhardt and Shaw, 2006).在快速伸长的根或黄化下胚轴细胞中, 周质微管表现为密集的横向平行排列(垂直于细胞的伸长方向) (Baskin et al., 2004).当植物根细胞中的周质微管排列方向由横向变为左手螺旋时, 植物根细胞则转变为右手螺旋方向生长, 即根由向下变为向右生长; 相反, 植物根细胞中的周质微管排列方向由横向变为右手螺旋时, 根细胞则转变为左手螺旋方向生长, 即根由向下变为向左生长(Furutani et al., 2000; Thitamadee et al., 2002; Nakajima et al., 2004). ...

Insensitivity to ethylene conferred by a dominant mutation in Arabidopsis thaliana
0
1988

Inhibition of cell expansion by rapid ABP1-mediated auxin effect on microtubules
1
2014

... 生长素促进下胚轴伸长可通过调节周质微管为横向排列实现.植株体内缺少生长素会抑制其生长, 细胞内的微管以纵向排列为主, 纵向排列的微管可通过外源添加生长素改变为横向排列, 且这种转变具有剂量依赖效应(Fischer and Schopfer, 1997).关于生长素信号调控微管骨架排列方式分子机制的研究, 从发现生长素能够调节下胚轴细胞内微管的重新排列就已开始.Chen等(2014)研究表明, 生长素通过生长素结合蛋白1 (auxin binding protein 1, ABP1)调节ROP (Rho of plants) GTPase、ROP的互作蛋白RIC1 (ROP-interactive CRIB motif-containing protein 1)和微管切割蛋白katanin来调控下胚轴细胞内的微管骨架重排.True和Shaw (2020)发现, 外源生长素诱导下胚轴细胞周质微管重排需要转运抑制因子/生长素F-box (transport inhibitor 1/auxin F-box, TIR1/AFB)转录途径.但是关于生长素促进下胚轴伸长与调控微管重排之间的关系尚存在不同观点, 有研究者认为, 下胚轴细胞内周质微管重排由生长本身引起, 而不依赖于生长素(Adamowski et al., 2019).目前, 在生长素调控下胚轴伸长过程中, 并未发现受生长素信号直接调控的微管蛋白或微管相关蛋白, 对于微管骨架响应生长素信号调节下胚轴伸长的机理也需深入研究. ...

Phenotypic and genetic analysis of det2, a new mutant that affects light- regulated seedling development in Arabidopsis
1
1991

... 油菜素甾醇(brassinosteroids, BRs)是一种重要的调节植物生长发育的植物激素(Clouse, 2011; Ye et al., 2011).BRs通过受体激酶BRI1 (brinsensitive1)以及特定的信号转导途径激活2个关键转录因子BZR1 (brassinazole-resistant 1)和BES1/BZR2 (brinsensi-tive1-EMS-suppressor1/brinsensitive2)来起作用(Li et al., 2010; Kim and Wang, 2010; Clouse, 2011; Gudesblat and Russinova, 2011).许多油菜素甾醇缺陷及不敏感突变体的黄化下胚轴变短且光下生长的植株矮小.例如, 油菜素甾醇合成缺失突变体det2 (de-etiolated-2)在黑暗下生长时子叶张开且下胚轴伸长受到抑制(Chory et al., 1991; Wang et al., 2001); 油菜素甾醇受体BRI1的无效突变体bri1-116植株也表现出黄化下胚轴短的表型; 油菜素甾醇信号途径转录因子BZR1的激活标签突变体bzr1-1D则表现出黄化下胚轴长且弯曲的表型; 油菜素甾醇信号途径的负调控因子BIN2的显性突变体bin2-1植株黄化下胚轴伸长也受到抑制; 油菜素甾醇信号通路中的上游组分BSKs和BSU1通过改变转录因子BZR1的磷酸化状态调控下胚轴的伸长(Tang et al., 2008; Kim et al., 2010; Gudesblat and Russinova, 2011).上述结果表明, BRs在调控下胚轴伸长方面起重要作用. ...

Brassinosteroid signal transduction: from receptor kinase activation to transcriptional networks regulating plant development
2
2011

... 油菜素甾醇(brassinosteroids, BRs)是一种重要的调节植物生长发育的植物激素(Clouse, 2011; Ye et al., 2011).BRs通过受体激酶BRI1 (brinsensitive1)以及特定的信号转导途径激活2个关键转录因子BZR1 (brassinazole-resistant 1)和BES1/BZR2 (brinsensi-tive1-EMS-suppressor1/brinsensitive2)来起作用(Li et al., 2010; Kim and Wang, 2010; Clouse, 2011; Gudesblat and Russinova, 2011).许多油菜素甾醇缺陷及不敏感突变体的黄化下胚轴变短且光下生长的植株矮小.例如, 油菜素甾醇合成缺失突变体det2 (de-etiolated-2)在黑暗下生长时子叶张开且下胚轴伸长受到抑制(Chory et al., 1991; Wang et al., 2001); 油菜素甾醇受体BRI1的无效突变体bri1-116植株也表现出黄化下胚轴短的表型; 油菜素甾醇信号途径转录因子BZR1的激活标签突变体bzr1-1D则表现出黄化下胚轴长且弯曲的表型; 油菜素甾醇信号途径的负调控因子BIN2的显性突变体bin2-1植株黄化下胚轴伸长也受到抑制; 油菜素甾醇信号通路中的上游组分BSKs和BSU1通过改变转录因子BZR1的磷酸化状态调控下胚轴的伸长(Tang et al., 2008; Kim et al., 2010; Gudesblat and Russinova, 2011).上述结果表明, BRs在调控下胚轴伸长方面起重要作用. ...

... ; Clouse, 2011; Gudesblat and Russinova, 2011).许多油菜素甾醇缺陷及不敏感突变体的黄化下胚轴变短且光下生长的植株矮小.例如, 油菜素甾醇合成缺失突变体det2 (de-etiolated-2)在黑暗下生长时子叶张开且下胚轴伸长受到抑制(Chory et al., 1991; Wang et al., 2001); 油菜素甾醇受体BRI1的无效突变体bri1-116植株也表现出黄化下胚轴短的表型; 油菜素甾醇信号途径转录因子BZR1的激活标签突变体bzr1-1D则表现出黄化下胚轴长且弯曲的表型; 油菜素甾醇信号途径的负调控因子BIN2的显性突变体bin2-1植株黄化下胚轴伸长也受到抑制; 油菜素甾醇信号通路中的上游组分BSKs和BSU1通过改变转录因子BZR1的磷酸化状态调控下胚轴的伸长(Tang et al., 2008; Kim et al., 2010; Gudesblat and Russinova, 2011).上述结果表明, BRs在调控下胚轴伸长方面起重要作用. ...

Gibberellins control Arabidopsis hypocotyl growth via regulation of cellular elongation
1
1999

... 赤霉素(gibberellin, GA)也参与调控植物下胚轴的伸长(Cowling and Harberd, 1999).GA可以促进黄瓜(Cucumis sativus)、生菜(Lactuca sativa var. ramosa)和拟南芥等植物下胚轴的伸长.外源添加赤霉素能促进光下生长的拟南芥下胚轴伸长, 但对黑暗下生长的下胚轴无促进效果, 这说明黑暗条件下下胚轴伸长对赤霉素的响应存在饱和效应(Sauret-Güeto et al., 2012).下胚轴伸长受光和赤霉素的拮抗作用(光抑制细胞伸长, 而赤霉素促进细胞伸长).具体调节机制为: 在光下, 光受体phyB介导光敏色素互作因子4 (PIF4)降解, PIF4调控的促进下胚轴细胞伸长的下游基因表达受到抑制, 进而抑制下胚轴伸长(Duek and Fankhauser, 2005; de Lucas et al., 2008).此外, 光使幼苗中赤霉素生物合成基因的表达瞬时下调, 编码赤霉素失活酶基因的表达上调, 因此可能导致活性赤霉素减少及DELLAs (赤霉素信号的负调控因子)蛋白在下胚轴细胞中积累(Peng et al., 1997; Silverstone et al., 1998; Reid et al., 2002; Achard et al., 2007; Alabadíet et al., 2008; Harberd et al., 2009).DELLA蛋白与促进细胞伸长的转录因子PIF3和PIF4互作抑制其活性, 进而使下胚轴伸长受到抑制.当赤霉素存在时, 赤霉素与受体结合, 促进受体与DELLA蛋白互作, 使DELLAs降解, PIF3和PIF4能发挥其转录活性, 进而促进下胚轴伸长(Feng et al., 2008; de Lucas et al., 2008). ...

Auxin, ethylene and brassinos-teroids: tripartite control of growth in theArabidopsis hy- pocotyl
1
2005

... 生长素(auxin)在控制细胞伸长过程中起重要作用.生长素的合成或运输受到影响均会改变拟南芥下胚轴的长度.生长素转运抑制剂NPA (1-naphthylphthala- mic acid)处理和生长素输出载体PIN1 (pin formed1)突变均可抑制光下下胚轴的伸长(Jensen et al., 1998; Friml et al., 2002), 而PIN1过表达可促进光下下胚轴的伸长(De Grauwe et al., 2005).外源施加生长素或上调生长素合成酶基因的表达都能促进光下生长的拟南芥下胚轴伸长, 黑暗下并无类似作用(Romano et al., 1995; Gray et al., 1998; van der Graaff et al., 2003).但也有研究表明, 提高生长素的水平会抑制黑暗下下胚轴的伸长.例如, 生长素合成酶基因YUCCA过表达植株, 光下下胚轴比野生型长而黑暗下下胚轴比野生型短, 说明在光暗两种条件下生长素可能发挥不同的作用或通过不同的信号途径发挥作用(Zhao et al., 2001). ...

A molecular framework for light and gibberellin control of cell elongation
2
2008

... 赤霉素(gibberellin, GA)也参与调控植物下胚轴的伸长(Cowling and Harberd, 1999).GA可以促进黄瓜(Cucumis sativus)、生菜(Lactuca sativa var. ramosa)和拟南芥等植物下胚轴的伸长.外源添加赤霉素能促进光下生长的拟南芥下胚轴伸长, 但对黑暗下生长的下胚轴无促进效果, 这说明黑暗条件下下胚轴伸长对赤霉素的响应存在饱和效应(Sauret-Güeto et al., 2012).下胚轴伸长受光和赤霉素的拮抗作用(光抑制细胞伸长, 而赤霉素促进细胞伸长).具体调节机制为: 在光下, 光受体phyB介导光敏色素互作因子4 (PIF4)降解, PIF4调控的促进下胚轴细胞伸长的下游基因表达受到抑制, 进而抑制下胚轴伸长(Duek and Fankhauser, 2005; de Lucas et al., 2008).此外, 光使幼苗中赤霉素生物合成基因的表达瞬时下调, 编码赤霉素失活酶基因的表达上调, 因此可能导致活性赤霉素减少及DELLAs (赤霉素信号的负调控因子)蛋白在下胚轴细胞中积累(Peng et al., 1997; Silverstone et al., 1998; Reid et al., 2002; Achard et al., 2007; Alabadíet et al., 2008; Harberd et al., 2009).DELLA蛋白与促进细胞伸长的转录因子PIF3和PIF4互作抑制其活性, 进而使下胚轴伸长受到抑制.当赤霉素存在时, 赤霉素与受体结合, 促进受体与DELLA蛋白互作, 使DELLAs降解, PIF3和PIF4能发挥其转录活性, 进而促进下胚轴伸长(Feng et al., 2008; de Lucas et al., 2008). ...

... ; de Lucas et al., 2008). ...

bHLH class transcription factors take centre stage in phytochrome signaling
1
2005

... 赤霉素(gibberellin, GA)也参与调控植物下胚轴的伸长(Cowling and Harberd, 1999).GA可以促进黄瓜(Cucumis sativus)、生菜(Lactuca sativa var. ramosa)和拟南芥等植物下胚轴的伸长.外源添加赤霉素能促进光下生长的拟南芥下胚轴伸长, 但对黑暗下生长的下胚轴无促进效果, 这说明黑暗条件下下胚轴伸长对赤霉素的响应存在饱和效应(Sauret-Güeto et al., 2012).下胚轴伸长受光和赤霉素的拮抗作用(光抑制细胞伸长, 而赤霉素促进细胞伸长).具体调节机制为: 在光下, 光受体phyB介导光敏色素互作因子4 (PIF4)降解, PIF4调控的促进下胚轴细胞伸长的下游基因表达受到抑制, 进而抑制下胚轴伸长(Duek and Fankhauser, 2005; de Lucas et al., 2008).此外, 光使幼苗中赤霉素生物合成基因的表达瞬时下调, 编码赤霉素失活酶基因的表达上调, 因此可能导致活性赤霉素减少及DELLAs (赤霉素信号的负调控因子)蛋白在下胚轴细胞中积累(Peng et al., 1997; Silverstone et al., 1998; Reid et al., 2002; Achard et al., 2007; Alabadíet et al., 2008; Harberd et al., 2009).DELLA蛋白与促进细胞伸长的转录因子PIF3和PIF4互作抑制其活性, 进而使下胚轴伸长受到抑制.当赤霉素存在时, 赤霉素与受体结合, 促进受体与DELLA蛋白互作, 使DELLAs降解, PIF3和PIF4能发挥其转录活性, 进而促进下胚轴伸长(Feng et al., 2008; de Lucas et al., 2008). ...

Microtubule dynamics and organization in the plant cortical array
2
2006

... 微管在植物多种生理活动中起重要作用, 如维持细胞形态、控制细胞极性生长、调控细胞有丝分裂与细胞分化以及参与囊泡运输和信号转导(Kost and Chua, 2002; Hashimoto, 2003; Lloyd and Chan, 2004; Hashimoto and Kato, 2006).4种微管列阵随着细胞周期依次转化, 执行相应的生理功能.其中, 周质微管列阵与植物细胞形态和生长方向等密切相关(Ehrhardt and Shaw, 2006).在快速伸长的根或黄化下胚轴细胞中, 周质微管表现为密集的横向平行排列(垂直于细胞的伸长方向) (Baskin et al., 2004).当植物根细胞中的周质微管排列方向由横向变为左手螺旋时, 植物根细胞则转变为右手螺旋方向生长, 即根由向下变为向右生长; 相反, 植物根细胞中的周质微管排列方向由横向变为右手螺旋时, 根细胞则转变为左手螺旋方向生长, 即根由向下变为向左生长(Furutani et al., 2000; Thitamadee et al., 2002; Nakajima et al., 2004). ...

... 乙烯是一种气体激素, 在调控植物下胚轴伸长中起重要作用(Smalle et al., 1997; Zhong et al., 2012).乙烯可根据光照条件促进或抑制拟南芥下胚轴伸长(Ecker et al.,1995; Smalle et al., 1997).光照条件下, 乙烯或者其前体ACC (1-aminocyclopropane-1-car-boxylic acid)处理可促进下胚轴伸长; 黑暗条件下, 乙烯则抑制下胚轴伸长(Zhong et al., 2012; Yu et al., 2013).乙烯通过转录因子EIN3激活PIF3依赖的生长促进途径及乙烯响应因子1 (ethylene response fac-tor 1, ERF1)介导的生长抑制途径来调控下胚轴生长.在光下, 乙烯通过其信号途径关键转录因子EIN3直接结合PIF3的启动子区激活其表达, 从而促进光下下胚轴伸长; 黑暗条件下, 乙烯可诱导抑制伸长的ERF1蛋白积累, 进而抑制黄化下胚轴伸长(Zhong et al., 2012).此外, 乙烯还可通过COP1介导的HY5 (hypocotyl 5)蛋白降解来促进光下下胚轴的伸长(Yu et al., 2013). ...

Coordi-nated regulation ofArabidopsis thaliana development by light and gibberellins
1
2008

... 赤霉素(gibberellin, GA)也参与调控植物下胚轴的伸长(Cowling and Harberd, 1999).GA可以促进黄瓜(Cucumis sativus)、生菜(Lactuca sativa var. ramosa)和拟南芥等植物下胚轴的伸长.外源添加赤霉素能促进光下生长的拟南芥下胚轴伸长, 但对黑暗下生长的下胚轴无促进效果, 这说明黑暗条件下下胚轴伸长对赤霉素的响应存在饱和效应(Sauret-Güeto et al., 2012).下胚轴伸长受光和赤霉素的拮抗作用(光抑制细胞伸长, 而赤霉素促进细胞伸长).具体调节机制为: 在光下, 光受体phyB介导光敏色素互作因子4 (PIF4)降解, PIF4调控的促进下胚轴细胞伸长的下游基因表达受到抑制, 进而抑制下胚轴伸长(Duek and Fankhauser, 2005; de Lucas et al., 2008).此外, 光使幼苗中赤霉素生物合成基因的表达瞬时下调, 编码赤霉素失活酶基因的表达上调, 因此可能导致活性赤霉素减少及DELLAs (赤霉素信号的负调控因子)蛋白在下胚轴细胞中积累(Peng et al., 1997; Silverstone et al., 1998; Reid et al., 2002; Achard et al., 2007; Alabadíet et al., 2008; Harberd et al., 2009).DELLA蛋白与促进细胞伸长的转录因子PIF3和PIF4互作抑制其活性, 进而使下胚轴伸长受到抑制.当赤霉素存在时, 赤霉素与受体结合, 促进受体与DELLA蛋白互作, 使DELLAs降解, PIF3和PIF4能发挥其转录活性, 进而促进下胚轴伸长(Feng et al., 2008; de Lucas et al., 2008). ...

Interaction of auxin, light, and mechanical stress in orienting microtubules in relation to tropic curvature in the epidermis of maize coleoptiles
1
1997

... 生长素促进下胚轴伸长可通过调节周质微管为横向排列实现.植株体内缺少生长素会抑制其生长, 细胞内的微管以纵向排列为主, 纵向排列的微管可通过外源添加生长素改变为横向排列, 且这种转变具有剂量依赖效应(Fischer and Schopfer, 1997).关于生长素信号调控微管骨架排列方式分子机制的研究, 从发现生长素能够调节下胚轴细胞内微管的重新排列就已开始.Chen等(2014)研究表明, 生长素通过生长素结合蛋白1 (auxin binding protein 1, ABP1)调节ROP (Rho of plants) GTPase、ROP的互作蛋白RIC1 (ROP-interactive CRIB motif-containing protein 1)和微管切割蛋白katanin来调控下胚轴细胞内的微管骨架重排.True和Shaw (2020)发现, 外源生长素诱导下胚轴细胞周质微管重排需要转运抑制因子/生长素F-box (transport inhibitor 1/auxin F-box, TIR1/AFB)转录途径.但是关于生长素促进下胚轴伸长与调控微管重排之间的关系尚存在不同观点, 有研究者认为, 下胚轴细胞内周质微管重排由生长本身引起, 而不依赖于生长素(Adamowski et al., 2019).目前, 在生长素调控下胚轴伸长过程中, 并未发现受生长素信号直接调控的微管蛋白或微管相关蛋白, 对于微管骨架响应生长素信号调节下胚轴伸长的机理也需深入研究. ...

Lateral relocation of auxin efflux regulator PIN3 mediates tropism in Arabidopsis
1
2002

... 生长素(auxin)在控制细胞伸长过程中起重要作用.生长素的合成或运输受到影响均会改变拟南芥下胚轴的长度.生长素转运抑制剂NPA (1-naphthylphthala- mic acid)处理和生长素输出载体PIN1 (pin formed1)突变均可抑制光下下胚轴的伸长(Jensen et al., 1998; Friml et al., 2002), 而PIN1过表达可促进光下下胚轴的伸长(De Grauwe et al., 2005).外源施加生长素或上调生长素合成酶基因的表达都能促进光下生长的拟南芥下胚轴伸长, 黑暗下并无类似作用(Romano et al., 1995; Gray et al., 1998; van der Graaff et al., 2003).但也有研究表明, 提高生长素的水平会抑制黑暗下下胚轴的伸长.例如, 生长素合成酶基因YUCCA过表达植株, 光下下胚轴比野生型长而黑暗下下胚轴比野生型短, 说明在光暗两种条件下生长素可能发挥不同的作用或通过不同的信号途径发挥作用(Zhao et al., 2001). ...

The SPIRAL genes are required for directional control of cell elongation in Arabidopsis thaliana
1
2000

... 微管在植物多种生理活动中起重要作用, 如维持细胞形态、控制细胞极性生长、调控细胞有丝分裂与细胞分化以及参与囊泡运输和信号转导(Kost and Chua, 2002; Hashimoto, 2003; Lloyd and Chan, 2004; Hashimoto and Kato, 2006).4种微管列阵随着细胞周期依次转化, 执行相应的生理功能.其中, 周质微管列阵与植物细胞形态和生长方向等密切相关(Ehrhardt and Shaw, 2006).在快速伸长的根或黄化下胚轴细胞中, 周质微管表现为密集的横向平行排列(垂直于细胞的伸长方向) (Baskin et al., 2004).当植物根细胞中的周质微管排列方向由横向变为左手螺旋时, 植物根细胞则转变为右手螺旋方向生长, 即根由向下变为向右生长; 相反, 植物根细胞中的周质微管排列方向由横向变为右手螺旋时, 根细胞则转变为左手螺旋方向生长, 即根由向下变为向左生长(Furutani et al., 2000; Thitamadee et al., 2002; Nakajima et al., 2004). ...

Cellular basis of hypocotyl growth in Arabidopsis thaliana
1
1997

... 下胚轴是高等植物的胚性器官, 指从子叶着生处以下生出的最初茎的部分.种子在土壤中萌发后, 下胚轴在黑暗条件下快速伸长以破土而出, 使子叶见光生长, 因此下胚轴伸长过程对于植物能否见光生长至关重要.拟南芥(Arabidopsis thaliana)作为模式植物, 其黑暗条件下生长的下胚轴(黄化下胚轴)为研究细胞伸长提供了良好的系统.拟南芥下胚轴由根(下)至子叶(上)一列表皮细胞的数目约为20个.黑暗条件下, 拟南芥下胚轴不同位置的细胞生长速率会随时间发生变化, 即下胚轴细胞的伸长表现出时空梯度特点.种子萌发后, 主要是靠近下胚轴基部的细胞伸长, 在黑暗条件下培养3天后, 靠近基部1-5个细胞的长度占整个下胚轴长度的一半; 继续黑暗培养至4-5天, 下胚轴基部的5个细胞伸长变慢, 中部的6-11个细胞以及上部的9个细胞快速伸长; 黑暗生长6天后, 中部及上部细胞生长速度减慢, 顶端弯钩处细胞伸长; 延长培养时间至7天后, 下胚轴细胞的伸长基本停滞(Gendreau et al., 1997), 表明黄化下胚轴细胞的伸长受时间和空间的精确调控. ...

High temperature promotes auxin-mediated hy-pocotyl elongation in Arabidopsis
1
1998

... 生长素(auxin)在控制细胞伸长过程中起重要作用.生长素的合成或运输受到影响均会改变拟南芥下胚轴的长度.生长素转运抑制剂NPA (1-naphthylphthala- mic acid)处理和生长素输出载体PIN1 (pin formed1)突变均可抑制光下下胚轴的伸长(Jensen et al., 1998; Friml et al., 2002), 而PIN1过表达可促进光下下胚轴的伸长(De Grauwe et al., 2005).外源施加生长素或上调生长素合成酶基因的表达都能促进光下生长的拟南芥下胚轴伸长, 黑暗下并无类似作用(Romano et al., 1995; Gray et al., 1998; van der Graaff et al., 2003).但也有研究表明, 提高生长素的水平会抑制黑暗下下胚轴的伸长.例如, 生长素合成酶基因YUCCA过表达植株, 光下下胚轴比野生型长而黑暗下下胚轴比野生型短, 说明在光暗两种条件下生长素可能发挥不同的作用或通过不同的信号途径发挥作用(Zhao et al., 2001). ...

Plants grow on bras-sinosteroids
2
2011

... 油菜素甾醇(brassinosteroids, BRs)是一种重要的调节植物生长发育的植物激素(Clouse, 2011; Ye et al., 2011).BRs通过受体激酶BRI1 (brinsensitive1)以及特定的信号转导途径激活2个关键转录因子BZR1 (brassinazole-resistant 1)和BES1/BZR2 (brinsensi-tive1-EMS-suppressor1/brinsensitive2)来起作用(Li et al., 2010; Kim and Wang, 2010; Clouse, 2011; Gudesblat and Russinova, 2011).许多油菜素甾醇缺陷及不敏感突变体的黄化下胚轴变短且光下生长的植株矮小.例如, 油菜素甾醇合成缺失突变体det2 (de-etiolated-2)在黑暗下生长时子叶张开且下胚轴伸长受到抑制(Chory et al., 1991; Wang et al., 2001); 油菜素甾醇受体BRI1的无效突变体bri1-116植株也表现出黄化下胚轴短的表型; 油菜素甾醇信号途径转录因子BZR1的激活标签突变体bzr1-1D则表现出黄化下胚轴长且弯曲的表型; 油菜素甾醇信号途径的负调控因子BIN2的显性突变体bin2-1植株黄化下胚轴伸长也受到抑制; 油菜素甾醇信号通路中的上游组分BSKs和BSU1通过改变转录因子BZR1的磷酸化状态调控下胚轴的伸长(Tang et al., 2008; Kim et al., 2010; Gudesblat and Russinova, 2011).上述结果表明, BRs在调控下胚轴伸长方面起重要作用. ...

... ; Gudesblat and Russinova, 2011).上述结果表明, BRs在调控下胚轴伸长方面起重要作用. ...

The angio- sperm gibberellin-GID1-DELLA growth regulatory mecha-nism: how an “inhibitor of an inhibitor” enables flexible response to fluctuating environments
1
2009

... 赤霉素(gibberellin, GA)也参与调控植物下胚轴的伸长(Cowling and Harberd, 1999).GA可以促进黄瓜(Cucumis sativus)、生菜(Lactuca sativa var. ramosa)和拟南芥等植物下胚轴的伸长.外源添加赤霉素能促进光下生长的拟南芥下胚轴伸长, 但对黑暗下生长的下胚轴无促进效果, 这说明黑暗条件下下胚轴伸长对赤霉素的响应存在饱和效应(Sauret-Güeto et al., 2012).下胚轴伸长受光和赤霉素的拮抗作用(光抑制细胞伸长, 而赤霉素促进细胞伸长).具体调节机制为: 在光下, 光受体phyB介导光敏色素互作因子4 (PIF4)降解, PIF4调控的促进下胚轴细胞伸长的下游基因表达受到抑制, 进而抑制下胚轴伸长(Duek and Fankhauser, 2005; de Lucas et al., 2008).此外, 光使幼苗中赤霉素生物合成基因的表达瞬时下调, 编码赤霉素失活酶基因的表达上调, 因此可能导致活性赤霉素减少及DELLAs (赤霉素信号的负调控因子)蛋白在下胚轴细胞中积累(Peng et al., 1997; Silverstone et al., 1998; Reid et al., 2002; Achard et al., 2007; Alabadíet et al., 2008; Harberd et al., 2009).DELLA蛋白与促进细胞伸长的转录因子PIF3和PIF4互作抑制其活性, 进而使下胚轴伸长受到抑制.当赤霉素存在时, 赤霉素与受体结合, 促进受体与DELLA蛋白互作, 使DELLAs降解, PIF3和PIF4能发挥其转录活性, 进而促进下胚轴伸长(Feng et al., 2008; de Lucas et al., 2008). ...

Dynamics and regulation of plant interphase microtubules: a comparative view
1
2003

... 微管在植物多种生理活动中起重要作用, 如维持细胞形态、控制细胞极性生长、调控细胞有丝分裂与细胞分化以及参与囊泡运输和信号转导(Kost and Chua, 2002; Hashimoto, 2003; Lloyd and Chan, 2004; Hashimoto and Kato, 2006).4种微管列阵随着细胞周期依次转化, 执行相应的生理功能.其中, 周质微管列阵与植物细胞形态和生长方向等密切相关(Ehrhardt and Shaw, 2006).在快速伸长的根或黄化下胚轴细胞中, 周质微管表现为密集的横向平行排列(垂直于细胞的伸长方向) (Baskin et al., 2004).当植物根细胞中的周质微管排列方向由横向变为左手螺旋时, 植物根细胞则转变为右手螺旋方向生长, 即根由向下变为向右生长; 相反, 植物根细胞中的周质微管排列方向由横向变为右手螺旋时, 根细胞则转变为左手螺旋方向生长, 即根由向下变为向左生长(Furutani et al., 2000; Thitamadee et al., 2002; Nakajima et al., 2004). ...

Cortical control of plant microtubules
2
2006

... 植物细胞骨架由微管和微丝组成.微管作为植物细胞骨架成员之一, 在植物生长发育过程中起重要作用(Hashimoto, 2003; Lloyd and Chan, 2004; Hashi- moto and Kato, 2006).下胚轴作为研究细胞伸长的模式器官, 其伸长既受到许多上游信号的调控也受到微管骨架的调节.早期关于下胚轴伸长的研究中, 细胞骨架和上游信号的调节处于相对独立状态.随着研究的不断深入, 发现微管受到上游信号的调控, 进而参与下胚轴伸长的调节.因此本文对近年来关于微管骨架响应环境和生长发育信号参与下胚轴伸长调节机制的研究进展进行了总结. ...

... 生长素(auxin)在控制细胞伸长过程中起重要作用.生长素的合成或运输受到影响均会改变拟南芥下胚轴的长度.生长素转运抑制剂NPA (1-naphthylphthala- mic acid)处理和生长素输出载体PIN1 (pin formed1)突变均可抑制光下下胚轴的伸长(Jensen et al., 1998; Friml et al., 2002), 而PIN1过表达可促进光下下胚轴的伸长(De Grauwe et al., 2005).外源施加生长素或上调生长素合成酶基因的表达都能促进光下生长的拟南芥下胚轴伸长, 黑暗下并无类似作用(Romano et al., 1995; Gray et al., 1998; van der Graaff et al., 2003).但也有研究表明, 提高生长素的水平会抑制黑暗下下胚轴的伸长.例如, 生长素合成酶基因YUCCA过表达植株, 光下下胚轴比野生型长而黑暗下下胚轴比野生型短, 说明在光暗两种条件下生长素可能发挥不同的作用或通过不同的信号途径发挥作用(Zhao et al., 2001). ...

Auxin transport is required for hypocotyl elongation in light-grown but not dark-grownArabidopsis
1
1998

... 油菜素甾醇(brassinosteroids, BRs)是一种重要的调节植物生长发育的植物激素(Clouse, 2011; Ye et al., 2011).BRs通过受体激酶BRI1 (brinsensitive1)以及特定的信号转导途径激活2个关键转录因子BZR1 (brassinazole-resistant 1)和BES1/BZR2 (brinsensi-tive1-EMS-suppressor1/brinsensitive2)来起作用(Li et al., 2010; Kim and Wang, 2010; Clouse, 2011; Gudesblat and Russinova, 2011).许多油菜素甾醇缺陷及不敏感突变体的黄化下胚轴变短且光下生长的植株矮小.例如, 油菜素甾醇合成缺失突变体det2 (de-etiolated-2)在黑暗下生长时子叶张开且下胚轴伸长受到抑制(Chory et al., 1991; Wang et al., 2001); 油菜素甾醇受体BRI1的无效突变体bri1-116植株也表现出黄化下胚轴短的表型; 油菜素甾醇信号途径转录因子BZR1的激活标签突变体bzr1-1D则表现出黄化下胚轴长且弯曲的表型; 油菜素甾醇信号途径的负调控因子BIN2的显性突变体bin2-1植株黄化下胚轴伸长也受到抑制; 油菜素甾醇信号通路中的上游组分BSKs和BSU1通过改变转录因子BZR1的磷酸化状态调控下胚轴的伸长(Tang et al., 2008; Kim et al., 2010; Gudesblat and Russinova, 2011).上述结果表明, BRs在调控下胚轴伸长方面起重要作用. ...

Constitutive activation of stress-inducible genes in a brassinosteroid-insensitive 1(bri1) mutant results in higher tolerance to cold
1
2010

... 油菜素甾醇(brassinosteroids, BRs)是一种重要的调节植物生长发育的植物激素(Clouse, 2011; Ye et al., 2011).BRs通过受体激酶BRI1 (brinsensitive1)以及特定的信号转导途径激活2个关键转录因子BZR1 (brassinazole-resistant 1)和BES1/BZR2 (brinsensi-tive1-EMS-suppressor1/brinsensitive2)来起作用(Li et al., 2010; Kim and Wang, 2010; Clouse, 2011; Gudesblat and Russinova, 2011).许多油菜素甾醇缺陷及不敏感突变体的黄化下胚轴变短且光下生长的植株矮小.例如, 油菜素甾醇合成缺失突变体det2 (de-etiolated-2)在黑暗下生长时子叶张开且下胚轴伸长受到抑制(Chory et al., 1991; Wang et al., 2001); 油菜素甾醇受体BRI1的无效突变体bri1-116植株也表现出黄化下胚轴短的表型; 油菜素甾醇信号途径转录因子BZR1的激活标签突变体bzr1-1D则表现出黄化下胚轴长且弯曲的表型; 油菜素甾醇信号途径的负调控因子BIN2的显性突变体bin2-1植株黄化下胚轴伸长也受到抑制; 油菜素甾醇信号通路中的上游组分BSKs和BSU1通过改变转录因子BZR1的磷酸化状态调控下胚轴的伸长(Tang et al., 2008; Kim et al., 2010; Gudesblat and Russinova, 2011).上述结果表明, BRs在调控下胚轴伸长方面起重要作用. ...

Brassinosteroid signal transduc-tion from receptor kinases to transcription factors
1
2010

... 微管在植物多种生理活动中起重要作用, 如维持细胞形态、控制细胞极性生长、调控细胞有丝分裂与细胞分化以及参与囊泡运输和信号转导(Kost and Chua, 2002; Hashimoto, 2003; Lloyd and Chan, 2004; Hashimoto and Kato, 2006).4种微管列阵随着细胞周期依次转化, 执行相应的生理功能.其中, 周质微管列阵与植物细胞形态和生长方向等密切相关(Ehrhardt and Shaw, 2006).在快速伸长的根或黄化下胚轴细胞中, 周质微管表现为密集的横向平行排列(垂直于细胞的伸长方向) (Baskin et al., 2004).当植物根细胞中的周质微管排列方向由横向变为左手螺旋时, 植物根细胞则转变为右手螺旋方向生长, 即根由向下变为向右生长; 相反, 植物根细胞中的周质微管排列方向由横向变为右手螺旋时, 根细胞则转变为左手螺旋方向生长, 即根由向下变为向左生长(Furutani et al., 2000; Thitamadee et al., 2002; Nakajima et al., 2004). ...

The plant cytoskeleton: vacuoles and cell walls make the difference
0
2002

Cell elongation and microtubule behavior in the Arabidopsis hypocotyl: responses to ethy- lene and auxin
3
2005

... 光是下胚轴伸长的主要调控因子之一.黑暗条件下, 植株下胚轴表现为黄化生长且快速伸长, 见光后下胚轴的伸长速率下降, 说明光对下胚轴伸长有强烈的抑制作用.Le等(2015)研究表明, 在快速伸长的下胚轴细胞内, 周质微管垂直于伸长轴, 表现为横向排列方式, 而在伸长缓慢或停止伸长的下胚轴细胞内, 周质微管表现为斜向或纵向排列; 快速伸长生长的黄化下胚轴见光后, 周质微管由横向平行排列变为斜向或纵向排列, 进而有利于抑制下胚轴的伸长.对光信号调节微管重排的研究发现, 光信号通过改变下胚轴细胞中周质微管的动态及转换能力调控其排列方式, 进而调节下胚轴的伸长.下胚轴细胞在快速伸长之前, 细胞内的微管会形成一种具有双极性的纵向列阵, 并转换为放射状的星状微管列阵, 之后开始进入快速伸长生长.在快速伸长的植株细胞内, 微管的聚合和重排速率都更快(Sambade et al., 2012).此外, 蓝光可在15分钟内诱导拟南芥下胚轴细胞中横向排列的周质微管完成90度重排.具体机理是: 蓝光照射后微管切割蛋白katanin切割交叉部位的微管产生新末端, 微管正端结合蛋白CLASP (cytoplasmic linker protein-associated protein)稳定新形成的微管末端, 使新末端在伸长过程中改变微管的排列方式为纵向排列(Lindeboom et al., 2013; Wang et al., 2017; Lindeboom et al., 2019) (表1).该研究结果为揭示光诱导微管重排的分子机理提供了重要线索. ...

... 此外, 还发现一些参与光信号调节微管重排的微管相关蛋白在下胚轴伸长中起重要作用, 但目前仍不清楚光信号如何调控这些微管相关蛋白.微管去稳定蛋白25 (microtubule destabilizing protein25, MDP 25)在光抑制下胚轴伸长中起重要作用.光信号引起下胚轴细胞中钙离子浓度增加, 使MDP25蛋白从质膜上脱离并进入细胞质, 通过调节周质微管从横向变为斜向或纵向排列, 在下胚轴由黑暗转移至光下后抑制光下下胚轴伸长过程中起重要作用(Li et al., 2011).Liu等(2013)发现了1个新的在光抑制下胚轴伸长过程中起正调控作用的微管相关蛋白WDL3 (wave-dampened2-like3).黑暗条件下, WDL3被26S蛋白酶体降解, 无法抑制下胚轴伸长, 而当黄化苗被转移至光下后, WDL3蛋白能稳定表达, 并通过调节下胚轴细胞内周质微管的组织动态抑制下胚轴伸长.Lian等(2017)研究发现, 黑暗条件下, 植物光形态建成的核心调控因子E3泛素连接酶COP1 (constitutive photomorphogenic1)可直接与WDL3结合并使其降解, 该研究揭示了光信号通过直接调控微管相关蛋白水平来调控周质微管重排的新机制.此外, 还有一些微管相关蛋白只特异性地在光下或黑暗下调节下胚轴的伸长.例如, 微管去稳定蛋白MDP60 (microtu bule destabilizing protein60)和微管稳定蛋白SPR1 (SPIRAL1).MDP60主要在下胚轴表达, 通过改变微管组织和动态来调节下胚轴伸长, 光通过其信号通路的核心转录因子PIF3 (phytochrome-interacting fac-tor 3)负调控MDP60的表达.PIF3作为乙烯促进光下下胚轴伸长的下游关键调节因子, 其蛋白水平受26S蛋白酶体对光信号响应的调节.在光介导的下胚轴伸长过程中, PIF3与MDP60启动子特异性结合, 从而提高MDP60的表达水平, MDP60通过改变微管排列促进下胚轴伸长(Ma et al., 2018).微管正端结合蛋白SPR1促进黑暗下生长的下胚轴细胞伸长, 在黑暗下生长的下胚轴中可检测到SPR1的表达, 而在光下生长的下胚轴中未检测到SPR1的表达, 表明光影响SPR1表达(Nakajima et al., 2004, 2006; Wang and Mao, 2019).但尚不清楚响应光调节SPR1表达的上游转录因子, 具体机理有待后续深入研究. ...

... ).Liu等(2013)发现了1个新的在光抑制下胚轴伸长过程中起正调控作用的微管相关蛋白WDL3 (wave-dampened2-like3).黑暗条件下, WDL3被26S蛋白酶体降解, 无法抑制下胚轴伸长, 而当黄化苗被转移至光下后, WDL3蛋白能稳定表达, 并通过调节下胚轴细胞内周质微管的组织动态抑制下胚轴伸长.Lian等(2017)研究发现, 黑暗条件下, 植物光形态建成的核心调控因子E3泛素连接酶COP1 (constitutive photomorphogenic1)可直接与WDL3结合并使其降解, 该研究揭示了光信号通过直接调控微管相关蛋白水平来调控周质微管重排的新机制.此外, 还有一些微管相关蛋白只特异性地在光下或黑暗下调节下胚轴的伸长.例如, 微管去稳定蛋白MDP60 (microtu bule destabilizing protein60)和微管稳定蛋白SPR1 (SPIRAL1).MDP60主要在下胚轴表达, 通过改变微管组织和动态来调节下胚轴伸长, 光通过其信号通路的核心转录因子PIF3 (phytochrome-interacting fac-tor 3)负调控MDP60的表达.PIF3作为乙烯促进光下下胚轴伸长的下游关键调节因子, 其蛋白水平受26S蛋白酶体对光信号响应的调节.在光介导的下胚轴伸长过程中, PIF3与MDP60启动子特异性结合, 从而提高MDP60的表达水平, MDP60通过改变微管排列促进下胚轴伸长(Ma et al., 2018).微管正端结合蛋白SPR1促进黑暗下生长的下胚轴细胞伸长, 在黑暗下生长的下胚轴中可检测到SPR1的表达, 而在光下生长的下胚轴中未检测到SPR1的表达, 表明光影响SPR1表达(Nakajima et al., 2004, 2006; Wang and Mao, 2019).但尚不清楚响应光调节SPR1表达的上游转录因子, 具体机理有待后续深入研究. ...

MDP25, a novel calcium regulatory protein, mediates hypocotyl cell elongation by destabilizing cortical microtubules in Ara- bidopsis
2
2011

... Representative microtubule-associated proteins that are involved in the hypocotyl elongation

Table 1

蛋白名称	对微管的调节	在下胚轴伸长中的作用	参考文献
Katanin	依赖ATP切割微管	通过蓝光刺激诱导, 在微管交叉部位切断微管, 产生新末端并迅速由横向变为纵向生长, 从而导致下胚轴细胞的生长方向改变	Lindeboom et al., 2013; Wang et al., 2017
CLASP	稳定微管正端	维持下胚轴正常生长, CLASP缺失突变体clasp-1下胚轴明显短于野生型	Ambrose et al., 2007
MDP25	解聚微管	作为下胚轴伸长的负调节因子, MDP25可直接与微管结合, 促进微管解聚, mdp25突变体的黄化下胚轴更长, 而MDP25过表达植株下胚轴较短	Li et al., 2011
WDL3	稳定并重排微管	黑暗下, WDL3被26S蛋白酶体降解, 促进下胚轴伸长; 光调节微管重排过程中, WDL3通过调节下胚轴细胞中微管成束抑制下胚轴伸长	Liu et al., 2013
MDP60	去稳定并重排微管	通过PIF3介导光和乙烯信号, 协同调控微管去稳定蛋白, 促进下胚轴伸长	Ma et al., 2018
SPR1	稳定微管	下胚轴伸长的正向调节因子SPR1在快速生长的下胚轴中高表达, 通过调节微管动态促进黑暗下下胚轴伸长	Nakajima et al., 2004, 2006
WDL5	稳定并重排微管	乙烯激活EIN3, EIN3直接调控WDL5上调表达, WDL5通过维持微管纵向排列抑制黄化下胚轴伸长	Sun et al., 2015
MDP40	去稳定并重排微管	油菜素甾醇激活BZR1, BZR1直接结合到MDP40的启动子上并上调其表达, MDP40解聚微管使其变为横向排列, 从而促进黄化下胚轴伸长	Wang et al., 2012

Table 1

蛋白名称	对微管的调节	在下胚轴伸长中的作用	参考文献
Katanin	依赖ATP切割微管	通过蓝光刺激诱导, 在微管交叉部位切断微管, 产生新末端并迅速由横向变为纵向生长, 从而导致下胚轴细胞的生长方向改变	Lindeboom et al., 2013; Wang et al., 2017
CLASP	稳定微管正端	维持下胚轴正常生长, CLASP缺失突变体clasp-1下胚轴明显短于野生型	Ambrose et al., 2007
MDP25	解聚微管	作为下胚轴伸长的负调节因子, MDP25可直接与微管结合, 促进微管解聚, mdp25突变体的黄化下胚轴更长, 而MDP25过表达植株下胚轴较短	Li et al., 2011
WDL3	稳定并重排微管	黑暗下, WDL3被26S蛋白酶体降解, 促进下胚轴伸长; 光调节微管重排过程中, WDL3通过调节下胚轴细胞中微管成束抑制下胚轴伸长	Liu et al., 2013
MDP60	去稳定并重排微管	通过PIF3介导光和乙烯信号, 协同调控微管去稳定蛋白, 促进下胚轴伸长	Ma et al., 2018
SPR1	稳定微管	下胚轴伸长的正向调节因子SPR1在快速生长的下胚轴中高表达, 通过调节微管动态促进黑暗下下胚轴伸长	Nakajima et al., 2004, 2006
WDL5	稳定并重排微管	乙烯激活EIN3, EIN3直接调控WDL5上调表达, WDL5通过维持微管纵向排列抑制黄化下胚轴伸长	Sun et al., 2015
MDP40	去稳定并重排微管	油菜素甾醇激活BZR1, BZR1直接结合到MDP40的启动子上并上调其表达, MDP40解聚微管使其变为横向排列, 从而促进黄化下胚轴伸长	Wang et al., 2012

Table 1

蛋白名称	对微管的调节	在下胚轴伸长中的作用	参考文献
Katanin	依赖ATP切割微管	通过蓝光刺激诱导, 在微管交叉部位切断微管, 产生新末端并迅速由横向变为纵向生长, 从而导致下胚轴细胞的生长方向改变	Lindeboom et al., 2013; Wang et al., 2017
CLASP	稳定微管正端	维持下胚轴正常生长, CLASP缺失突变体clasp-1下胚轴明显短于野生型	Ambrose et al., 2007
MDP25	解聚微管	作为下胚轴伸长的负调节因子, MDP25可直接与微管结合, 促进微管解聚, mdp25突变体的黄化下胚轴更长, 而MDP25过表达植株下胚轴较短	Li et al., 2011
WDL3	稳定并重排微管	黑暗下, WDL3被26S蛋白酶体降解, 促进下胚轴伸长; 光调节微管重排过程中, WDL3通过调节下胚轴细胞中微管成束抑制下胚轴伸长	Liu et al., 2013
MDP60	去稳定并重排微管	通过PIF3介导光和乙烯信号, 协同调控微管去稳定蛋白, 促进下胚轴伸长	Ma et al., 2018
SPR1	稳定微管	下胚轴伸长的正向调节因子SPR1在快速生长的下胚轴中高表达, 通过调节微管动态促进黑暗下下胚轴伸长	Nakajima et al., 2004, 2006
WDL5	稳定并重排微管	乙烯激活EIN3, EIN3直接调控WDL5上调表达, WDL5通过维持微管纵向排列抑制黄化下胚轴伸长	Sun et al., 2015
MDP40	去稳定并重排微管	油菜素甾醇激活BZR1, BZR1直接结合到MDP40的启动子上并上调其表达, MDP40解聚微管使其变为横向排列, 从而促进黄化下胚轴伸长	Wang et al., 2012

Table 1

蛋白名称	对微管的调节	在下胚轴伸长中的作用	参考文献
Katanin	依赖ATP切割微管	通过蓝光刺激诱导, 在微管交叉部位切断微管, 产生新末端并迅速由横向变为纵向生长, 从而导致下胚轴细胞的生长方向改变	Lindeboom et al., 2013; Wang et al., 2017
CLASP	稳定微管正端	维持下胚轴正常生长, CLASP缺失突变体clasp-1下胚轴明显短于野生型	Ambrose et al., 2007
MDP25	解聚微管	作为下胚轴伸长的负调节因子, MDP25可直接与微管结合, 促进微管解聚, mdp25突变体的黄化下胚轴更长, 而MDP25过表达植株下胚轴较短	Li et al., 2011
WDL3	稳定并重排微管	黑暗下, WDL3被26S蛋白酶体降解, 促进下胚轴伸长; 光调节微管重排过程中, WDL3通过调节下胚轴细胞中微管成束抑制下胚轴伸长	Liu et al., 2013
MDP60	去稳定并重排微管	通过PIF3介导光和乙烯信号, 协同调控微管去稳定蛋白, 促进下胚轴伸长	Ma et al., 2018
SPR1	稳定微管	下胚轴伸长的正向调节因子SPR1在快速生长的下胚轴中高表达, 通过调节微管动态促进黑暗下下胚轴伸长	Nakajima et al., 2004, 2006
WDL5	稳定并重排微管	乙烯激活EIN3, EIN3直接调控WDL5上调表达, WDL5通过维持微管纵向排列抑制黄化下胚轴伸长	Sun et al., 2015
MDP40	去稳定并重排微管	油菜素甾醇激活BZR1, BZR1直接结合到MDP40的启动子上并上调其表达, MDP40解聚微管使其变为横向排列, 从而促进黄化下胚轴伸长	Wang et al., 2012

Table 1

蛋白名称	对微管的调节	在下胚轴伸长中的作用	参考文献
Katanin	依赖ATP切割微管	通过蓝光刺激诱导, 在微管交叉部位切断微管, 产生新末端并迅速由横向变为纵向生长, 从而导致下胚轴细胞的生长方向改变	Lindeboom et al., 2013; Wang et al., 2017
CLASP	稳定微管正端	维持下胚轴正常生长, CLASP缺失突变体clasp-1下胚轴明显短于野生型	Ambrose et al., 2007
MDP25	解聚微管	作为下胚轴伸长的负调节因子, MDP25可直接与微管结合, 促进微管解聚, mdp25突变体的黄化下胚轴更长, 而MDP25过表达植株下胚轴较短	Li et al., 2011
WDL3	稳定并重排微管	黑暗下, WDL3被26S蛋白酶体降解, 促进下胚轴伸长; 光调节微管重排过程中, WDL3通过调节下胚轴细胞中微管成束抑制下胚轴伸长	Liu et al., 2013
MDP60	去稳定并重排微管	通过PIF3介导光和乙烯信号, 协同调控微管去稳定蛋白, 促进下胚轴伸长	Ma et al., 2018
SPR1	稳定微管	下胚轴伸长的正向调节因子SPR1在快速生长的下胚轴中高表达, 通过调节微管动态促进黑暗下下胚轴伸长	Nakajima et al., 2004, 2006
WDL5	稳定并重排微管	乙烯激活EIN3, EIN3直接调控WDL5上调表达, WDL5通过维持微管纵向排列抑制黄化下胚轴伸长	Sun et al., 2015
MDP40	去稳定并重排微管	油菜素甾醇激活BZR1, BZR1直接结合到MDP40的启动子上并上调其表达, MDP40解聚微管使其变为横向排列, 从而促进黄化下胚轴伸长	Wang et al., 2012

Table 1

蛋白名称	对微管的调节	在下胚轴伸长中的作用	参考文献
Katanin	依赖ATP切割微管	通过蓝光刺激诱导, 在微管交叉部位切断微管, 产生新末端并迅速由横向变为纵向生长, 从而导致下胚轴细胞的生长方向改变	Lindeboom et al., 2013; Wang et al., 2017
CLASP	稳定微管正端	维持下胚轴正常生长, CLASP缺失突变体clasp-1下胚轴明显短于野生型	Ambrose et al., 2007
MDP25	解聚微管	作为下胚轴伸长的负调节因子, MDP25可直接与微管结合, 促进微管解聚, mdp25突变体的黄化下胚轴更长, 而MDP25过表达植株下胚轴较短	Li et al., 2011
WDL3	稳定并重排微管	黑暗下, WDL3被26S蛋白酶体降解, 促进下胚轴伸长; 光调节微管重排过程中, WDL3通过调节下胚轴细胞中微管成束抑制下胚轴伸长	Liu et al., 2013
MDP60	去稳定并重排微管	通过PIF3介导光和乙烯信号, 协同调控微管去稳定蛋白, 促进下胚轴伸长	Ma et al., 2018
SPR1	稳定微管	下胚轴伸长的正向调节因子SPR1在快速生长的下胚轴中高表达, 通过调节微管动态促进黑暗下下胚轴伸长	Nakajima et al., 2004, 2006
WDL5	稳定并重排微管	乙烯激活EIN3, EIN3直接调控WDL5上调表达, WDL5通过维持微管纵向排列抑制黄化下胚轴伸长	Sun et al., 2015
MDP40	去稳定并重排微管	油菜素甾醇激活BZR1, BZR1直接结合到MDP40的启动子上并上调其表达, MDP40解聚微管使其变为横向排列, 从而促进黄化下胚轴伸长	Wang et al., 2012

Table 1

蛋白名称	对微管的调节	在下胚轴伸长中的作用	参考文献
Katanin	依赖ATP切割微管	通过蓝光刺激诱导, 在微管交叉部位切断微管, 产生新末端并迅速由横向变为纵向生长, 从而导致下胚轴细胞的生长方向改变	Lindeboom et al., 2013; Wang et al., 2017
CLASP	稳定微管正端	维持下胚轴正常生长, CLASP缺失突变体clasp-1下胚轴明显短于野生型	Ambrose et al., 2007
MDP25	解聚微管	作为下胚轴伸长的负调节因子, MDP25可直接与微管结合, 促进微管解聚, mdp25突变体的黄化下胚轴更长, 而MDP25过表达植株下胚轴较短	Li et al., 2011
WDL3	稳定并重排微管	黑暗下, WDL3被26S蛋白酶体降解, 促进下胚轴伸长; 光调节微管重排过程中, WDL3通过调节下胚轴细胞中微管成束抑制下胚轴伸长	Liu et al., 2013
MDP60	去稳定并重排微管	通过PIF3介导光和乙烯信号, 协同调控微管去稳定蛋白, 促进下胚轴伸长	Ma et al., 2018
SPR1	稳定微管	下胚轴伸长的正向调节因子SPR1在快速生长的下胚轴中高表达, 通过调节微管动态促进黑暗下下胚轴伸长	Nakajima et al., 2004, 2006
WDL5	稳定并重排微管	乙烯激活EIN3, EIN3直接调控WDL5上调表达, WDL5通过维持微管纵向排列抑制黄化下胚轴伸长	Sun et al., 2015
MDP40	去稳定并重排微管	油菜素甾醇激活BZR1, BZR1直接结合到MDP40的启动子上并上调其表达, MDP40解聚微管使其变为横向排列, 从而促进黄化下胚轴伸长	Wang et al., 2012

Table 1

蛋白名称	对微管的调节	在下胚轴伸长中的作用	参考文献
Katanin	依赖ATP切割微管	通过蓝光刺激诱导, 在微管交叉部位切断微管, 产生新末端并迅速由横向变为纵向生长, 从而导致下胚轴细胞的生长方向改变	Lindeboom et al., 2013; Wang et al., 2017
CLASP	稳定微管正端	维持下胚轴正常生长, CLASP缺失突变体clasp-1下胚轴明显短于野生型	Ambrose et al., 2007
MDP25	解聚微管	作为下胚轴伸长的负调节因子, MDP25可直接与微管结合, 促进微管解聚, mdp25突变体的黄化下胚轴更长, 而MDP25过表达植株下胚轴较短	Li et al., 2011
WDL3	稳定并重排微管	黑暗下, WDL3被26S蛋白酶体降解, 促进下胚轴伸长; 光调节微管重排过程中, WDL3通过调节下胚轴细胞中微管成束抑制下胚轴伸长	Liu et al., 2013
MDP60	去稳定并重排微管	通过PIF3介导光和乙烯信号, 协同调控微管去稳定蛋白, 促进下胚轴伸长	Ma et al., 2018
SPR1	稳定微管	下胚轴伸长的正向调节因子SPR1在快速生长的下胚轴中高表达, 通过调节微管动态促进黑暗下下胚轴伸长	Nakajima et al., 2004, 2006
WDL5	稳定并重排微管	乙烯激活EIN3, EIN3直接调控WDL5上调表达, WDL5通过维持微管纵向排列抑制黄化下胚轴伸长	Sun et al., 2015
MDP40	去稳定并重排微管	油菜素甾醇激活BZR1, BZR1直接结合到MDP40的启动子上并上调其表达, MDP40解聚微管使其变为横向排列, 从而促进黄化下胚轴伸长	Wang et al., 2012

Table 1

蛋白名称	对微管的调节	在下胚轴伸长中的作用	参考文献
Katanin	依赖ATP切割微管	通过蓝光刺激诱导, 在微管交叉部位切断微管, 产生新末端并迅速由横向变为纵向生长, 从而导致下胚轴细胞的生长方向改变	Lindeboom et al., 2013; Wang et al., 2017
CLASP	稳定微管正端	维持下胚轴正常生长, CLASP缺失突变体clasp-1下胚轴明显短于野生型	Ambrose et al., 2007
MDP25	解聚微管	作为下胚轴伸长的负调节因子, MDP25可直接与微管结合, 促进微管解聚, mdp25突变体的黄化下胚轴更长, 而MDP25过表达植株下胚轴较短	Li et al., 2011
WDL3	稳定并重排微管	黑暗下, WDL3被26S蛋白酶体降解, 促进下胚轴伸长; 光调节微管重排过程中, WDL3通过调节下胚轴细胞中微管成束抑制下胚轴伸长	Liu et al., 2013
MDP60	去稳定并重排微管	通过PIF3介导光和乙烯信号, 协同调控微管去稳定蛋白, 促进下胚轴伸长	Ma et al., 2018
SPR1	稳定微管	下胚轴伸长的正向调节因子SPR1在快速生长的下胚轴中高表达, 通过调节微管动态促进黑暗下下胚轴伸长	Nakajima et al., 2004, 2006
WDL5	稳定并重排微管	乙烯激活EIN3, EIN3直接调控WDL5上调表达, WDL5通过维持微管纵向排列抑制黄化下胚轴伸长	Sun et al., 2015
MDP40	去稳定并重排微管	油菜素甾醇激活BZR1, BZR1直接结合到MDP40的启动子上并上调其表达, MDP40解聚微管使其变为横向排列, 从而促进黄化下胚轴伸长	Wang et al., 2012