独脚金内酯调控植物侧枝发育的分子机制及其与生长素交互作用的研究进展

对独脚金内酯（strigolactones,SLs）调控植物侧枝发育的分子机制及其与生长素相互作用的相关研究结果进行了总结和归纳,在此基础上提出今后的重点研究方向。相关的研究结果显示：在拟南芥[Arabidops~thaliana（Linn．）Heynh．]、豌豆（Pisum sativum Linn．）和水稻（Oryza sativa Linn．）等植物多枝突变体中SLs作为可转导信号参与侧枝发育的分子调控,从这些植物中已克隆获得参与SLs生物合成及信号应答途径的一些基因。作为一种植物激素,SLs在侧枝发育调控网络中与生长素相互作用;腋芽发育与其中生长素的输出密切相关,SLs通过调控芽中生长素的输出间接抑制腋芽发育和侧枝生长,而生长素则在SLs生物合成中起调节作用。     

表观遗传调控植物分枝/分蘖研究进展

分蘖是禾本科植物特有的分枝类型, 是影响作物产量的关键因素之一。分枝/分蘖数由叶腋处侧生分生组织的数量和侧芽的活性共同决定。表观遗传修饰调控植物生长发育的各个方面, 但是如何调控植物的分枝/分蘖数还未见系统报道。该综述归纳了表观遗传调控侧生分生组织的形成和侧芽向外生长两个方面, 并展望了表观遗传在调控植物分枝/分蘖中的研究方向, 以期为通过表观遗传修饰改良作物品种的育种途径提供理论指导。     

生长素调控植物株型形成的研究进展

高等植物通过调节顶端分生组织和侧生分生组织的活性建立地上株型系统,分生组织的活性受环境信号、发育阶段和遗传因素的综合调控,植物激素参与这些信号的整合。顶端优势是植物分枝调控的核心问题,而生长素对顶端优势的形成和维持发挥关键作用。本文综述了近几年与植物地上部分株型形成相关的生长素合成代谢、极性运输及信号转导领域的研究进展,并提出了展望。     

生长素调控植物株型形成的研究进展

高等植物通过调节顶端分生组织和侧生分生组织的活性建立地上株型系统, 分生组织的活性受环境信号、发育阶段和遗传因素的综合调控, 植物激素参与这些信号的整合。顶端优势是植物分枝调控的核心问题, 而生长素对顶端优势的形成和维持发挥关键作用。本文综述了近几年与植物地上部分株型形成相关的生长素合成代谢、极性运输及信号转导领域的研究进展, 并提出了展望。     

植物的次生生长及其分子调控

植物的次生生长是一重要的生命活动, 特别是植物次生木质部的形成对人类生产和生活具有重大意义。次生生长包括维管组织形成、次生细胞壁形成、木质化、PCD以及心材形成等过程。生长素和多个转录因子家族如MYB、NAC、AP2/EREBP、homeobox、MADS等参与了这一过程的调控, 利用分子生物学手段特别是基因组学方法, 人们已分离到生长素信号途径基因以及转录因子家族中的相关调控基因。文章介绍了植物次生生长的活动过程, 并论述了次生生长过程中调控基因的研究情况。     

植物生长素反应因子研究进展

生长素反应因子（ARFs）是植物生长和发育的重要调节因子,在生长素早期反应蛋白（Aux／IAAs）的参与下,通过和生长素反应基因启动子区AuxRE元件的JTGTCTC序列结合,共同调控这些基因的表达。近年来关于生长素反应因子的分子结构和ARF与Aux／IAA的相互作用及其对植物生长和发育的影响、作用的靶基因以及分子机制受到人们的重视,并在这些方面做了大量的研究。     

FT及其同源基因在植物发育调控中的多功能效应

FT是植物开花调控途径的重要整合因子和调控开花的关键基因之一,也是植物可传导开花物质“成花素”的编码基因.FT蛋白是成花素的必需组分,FT mRNA是成花素的潜在组分;FT及其同源基因不仅参与株龄影响及逆境诱导的开花,还参与营养生长、器官形态建成、源库关系和器官脱落调控.该文对近年来国内外有关FT及其同源基因在植物发育调控中的多种功能效应及作用方式进行综述.     

独脚金内酯调控侧枝发育的研究进展

植物通过内源激素或环境信号调控叶腋内腋芽的形成和发育,从而控制其分枝特性。独脚金内酯(strigolactones,SLs),一种产生于植物根部的类胡萝卜素衍生物,具有刺激寄生植物种子的萌发和促进丛枝菌根真菌菌丝分枝的作用,最近的研究表明,它还可以沿茎干向上运输,与生长素和细胞分裂素一起直接或间接抑制植物分枝,目前已经作为一种新的植物激素受到广泛认可。本文综述了独脚金内酯的结构、合成途径和生物活性,以及调控植物分枝的分子机理,并展望了其在抑制杂草或新型除草剂的研发、促进植物和有益真菌的共生,以及调控作物的分枝和株型等方面的应用前景。     

WOX蛋白家族调控干细胞发育分子机制的研究进展

WOX蛋白家族是植物特有的一类转录因子家族, 是植物胚胎建成、干细胞维持和器官发生等发育过程中的重要调控因子。越来越多的研究表明, 作为干细胞维持的关键因子之一, WOX蛋白家族通过相似或特异的调控网络参与植物初生分生组织(茎尖和根尖分生组织)和次生分生组织(维管分生组织)等各级干细胞的维持和分化。该文综述了近年来WOX蛋白家族调控干细胞发育分子机制的研究进展, 并对其在单、双子叶植物中功能的保守性进行了比较和分析。     

烟草NtMAX4-1基因的克隆及特征分析

类胡萝卜素裂解双加氧酶8(CCD8或MAX4)在独脚金内酯合成中发挥重要作用,进而调控植物侧枝的发生。烟草生产过程中,控制腋芽是一项基本的措施。克隆腋芽控制基因从分子水平上为研究腋芽萌发和抑制其生长提供了靶标。本研究克隆了烟草Nt MAX4-1基因的全长c DNA,对其编码蛋白的理论等电点、分子质量、二级结构、亚细胞定位等特性进行了预测。Nt MAX4-1蛋白含有MAX4蛋白特有的视网膜色素上皮细胞膜蛋白保守结构域,多序列比对及进化树分析表明Nt MAX4-1蛋白与番茄MAX4蛋白遗传距离最近。另外,对Nt MAX4-1基因的组织特异性表达进行了分析,结果表明,Nt MAX4-1在烟草茎中表达量最高,根中次之,叶和花中基本检测不到。     

The Arabidopsis MAX pathway controls shoot branching by regulating auxin transport

BACKGROUND: Plants achieve remarkable plasticity in shoot system architecture by regulating the activity of secondary shoot meristems, laid down in the axil of each leaf. Axillary meristem activity, and hence shoot branching, is regulated by a network of interacting hormonal signals that move through the plant. Among these, auxin, moving down the plant in the main stem, indirectly inhibits axillary bud outgrowth, and an as yet undefined hormone, the synthesis of which in Arabidopsis requires MAX1, MAX3, and MAX4, moves up the plant and also inhibits shoot branching. Since the axillary buds of max4 mutants are resistant to the inhibitory effects of apically supplied auxin, auxin and the MAX-dependent hormone must interact to inhibit branching. RESULTS: Here we show that the resistance of max mutant buds to apically supplied auxin is largely independent of the known, AXR1-mediated, auxin signal transduction pathway. Instead, it is caused by increased capacity for auxin transport in max primary stems, which show increased expression of PIN auxin efflux facilitators. The max phenotype is dependent on PIN1 activity, but it is independent of flavonoids, which are known regulators of PIN-dependent auxin transport. CONCLUSIONS: The MAX-dependent hormone is a novel regulator of auxin transport. Modulation of auxin transport in the stem is sufficient to regulate bud outgrowth, independent of AXR1-mediated auxin signaling. We therefore propose an additional mechanism for long-range signaling by auxin in which bud growth is regulated by competition between auxin sources for auxin transport capacity in the primary stem.     

Hormonal control of shoot branching

Shoot branching is the process by which axillary buds, located on the axil of a leaf, develop and form new flowers or branches. The process by which a dormant bud activates and becomes an actively growing branch is complex and very finely tuned. Bud outgrowth is regulated by the interaction of environmental signals and endogenous ones, such as plant hormones. Thus these interacting factors have a major effect on shoot system architecture. Hormones known to have a major influence are auxin, cytokinin, and a novel, as yet chemically undefined, hormone. Auxin is actively transported basipetally in the shoot and inhibits bud outgrowth. By contrast, cytokinins travel acropetally and promote bud outgrowth. The novel hormone also moves acropetally but it inhibits bud outgrowth. The aim of this review is to integrate what is known about the hormonal control of shoot branching in Arabidopsis, focusing on these three hormones and their interactions.     

Roles for Auxin, Cytokinin, and Strigolactone in Regulating Shoot Branching

Many processes have been described in the control of shoot branching. Apical dominance is defined as the control exerted by the shoot tip on the outgrowth of axillary buds, whereas correlative inhibition includes the suppression of growth by other growing buds or shoots. The level, signaling, and/or flow of the plant hormone auxin in stems and buds is thought to be involved in these processes. In addition, RAMOSUS (RMS) branching genes in pea (Pisum sativum) control the synthesis and perception of a long-distance inhibitory branching signal produced in the stem and roots, a strigolactone or product. Auxin treatment affects the expression of RMS genes, but it is unclear whether the RMS network can regulate branching independently of auxin. Here, we explore whether apical dominance and correlative inhibition show independent or additive effects in rms mutant plants. Bud outgrowth and branch lengths are enhanced in decapitated and stem-girdled rms mutants compared with intact control plants. This may relate to an RMS-independent induction of axillary bud outgrowth by these treatments. Correlative inhibition was also apparent in rms mutant plants, again indicating an RMS-independent component. Treatments giving reductions in RMS1 and RMS5 gene expression, auxin transport, and auxin level in the main stem were not always sufficient to promote bud outgrowth. We suggest that this may relate to a failure to induce the expression of cytokinin biosynthesis genes, which always correlated with bud outgrowth in our treatments. We present a new model that accounts for apical dominance, correlative inhibition, RMS gene action, and auxin and cytokinin and their interactions in controlling the progression of buds through different control points from dormancy to sustained growth.     

Auxin–cytokinin interactions in the control of shoot branching

In many plant species, the intact main shoot apex grows predominantly and axillary bud outgrowth is inhibited. This phenomenon is called apical dominance, and has been analyzed for over 70 years. Decapitation of the shoot apex releases the axillary buds from their dormancy and they begin to grow out. Auxin derived from an intact shoot apex suppresses axillary bud outgrowth, whereas cytokinin induced by decapitation of the shoot apex stimulates axillary bud outgrowth. Here we describe the molecular mechanisms of the interactions between auxin and cytokinin in the control of shoot branching.     

Photosynthetic leaf area modulates tiller bud outgrowth in sorghum

Shoot branches or tillers develop from axillary buds. The dormancy versus outgrowth fates of buds depends on genetic, environmental and hormonal signals. Defoliation inhibits bud outgrowth indicating the role of leaf‐derived metabolic factors such as sucrose in bud outgrowth. In this study, the sensitivity of bud outgrowth to selective defoliation was investigated. At 6 d after planting (6 DAP), the first two leaves of sorghum were fully expanded and the third was partially emerged. Therefore, the leaves were selectively defoliated at 6 DAP and the length of the bud in the first leaf axil was measured at 8 DAP. Bud outgrowth was inhibited by defoliation of only 2 cm from the tip of the second leaf blade. The expression of dormancy and sucrose‐starvation marker genes was up‐regulated and cell cycle and sucrose‐inducible genes was down‐regulated during the first 24 h post‐defoliation of the second leaf. At 48 h, the expression of these genes was similar to controls as the defoliated plant recovers. Our results demonstrate that small changes in photosynthetic leaf area affect the propensity of tiller buds for outgrowth. Therefore, variation in leaf area and photosynthetic activity should be included when integrating sucrose into models of shoot branching.