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.     

烟草BRANCHED1-Like基因的克隆及表达分析

TCP基因家族CYC/TB1簇中成员BRC1在调控植物侧枝发育的过程中发挥重要作用。本研究利用电子克隆的策略结合RT-PCR方法从普通烟草（Nicotiana tabacum）中克隆到4个NtBRC1-Like基因,分别命名为NtBRC1-Like1、2、3和4。4条基因的CDS序列长度分别为1140、1062、987和1041bp,分别编码由379、353、328和346个氨基酸组成的蛋白,这4个蛋白与CYC/TB1簇中其它成员具有较高同源性。蛋白质保守结构域分析表明,4个NtBRC1-Like基因编码蛋白除具有TCP核心结构域外,还具有CYC/TB1簇蛋白特有的R结构域。系统进化树分析表明,NtBRC1-Like蛋白都是TCP家族CYC/TB1簇中的成员,且4个NtBRC1-Like蛋白可以被分成两组,NtBRC1-Like1和4为一组,NtBRC1-Like2和3为另一组。荧光定量PCR分析发现,4条烟草NtBRC1-Like基因的表达呈现明显的组织特异性,且其表达模式可分为两种：NtBRC1-Like1和4的表达模式相似,在腋芽中有极高的表达;NtBRC1-Like2和3的表达模式十分相像,在叶和腋芽中的表达量都显著高于其它组织。推测烟草BRC1基因可能存在类似番茄BRC1基因在功能上保守与进化的情况。     

Overexpression of a NAC-domain protein promotes shoot branching in rice

For a better understanding of shoot branching in rice (Oryza sativa), a rice activation-tagging library was screened for mutations in tiller development. Here, an activation-tagging mutant Ostil1 (Oryza sativa tillering1) was characterized, which showed increased tillers, enlarged tiller angle and semidwarf phenotype. Flanking sequence was obtained by plasmid rescue. RNA-interfering and overexpression transgenic rice plants were produced using Agrobacterium-mediated transformation. The mutant phenotype was cosegregated with the reallocation of Ds element, and the flanking region of the reallocated Ds element was identified as part of the OsNAC2 gene. Northern analysis showed that expression of OsNAC2 was greatly induced in the mutant plants. Transgenic rice overexpressing the OsNAC2 resulted in recapture of the mutant phenotype, while downregulation of OsNAC2 in the Ostil1 mutant through RNA interfering (RNAi) complemented the mutant phenotype, confirming that the Ostil1 was caused by overexpression of OsNAC2. Overexpression of OsNAC2 regulates shoot branching in rice. Overexpression of OsNAC2 contributes tiller bud outgrowth, but does not affect tiller bud initiation. This suggests that OsNAC2 has potential utility for improving plant structure for higher light-use efficiency and higher yield potential in rice.     

Auxin, cytokinin and the control of shoot branching

BACKGROUND: It has been known for many decades that auxin inhibits the activation of axillary buds, and hence shoot branching, while cytokinin has the opposite effect. However, the modes of action of these two hormones in branching control is still a matter of debate, and their mechanisms of interaction are equally unresolved. SCOPE: Here we review the evidence for various hypotheses that have been put forward to explain how auxin and cytokinin influence axillary bud activity. In particular we discuss the roles of auxin and cytokinin in regulating each other's synthesis, the cell cycle, meristem function and auxin transport, each of which could affect branching. These different mechanisms have implications for the main site of hormone action, ranging from systemic action throughout the plant, to local action at the node or in the bud meristem or leaves. The alternative models have specific predictions, and our increasing understanding of the molecular basis for hormone transport and signalling, cell cycle control and meristem biology is providing new tools to enable these predictions to be tested.     

Strigolactones are a new-defined class of plant hormones which inhibit shoot branching and mediate the interaction of plant-AM fungi and plant-parasitic weeds

Because plants are sessile organisms, the ability to adapt to a wide range of environmental conditions is critical for their survival. As a consequence, plants use hormones to regulate growth, mitigate biotic and abiotic stresses, and to communicate with other organisms. Many plant hormones function plei-otropically in vivo, and often work in tandem with other hormones that are chemically distinct. A newly-defined class of plant hormones, the strigolactones, cooperate with auxins and cytokinins to control shoot branching and the outgrowth of lateral buds. Strigolactones were originally identified as compounds that stimulated the germination of parasitic plant seeds, and were also demonstrated to induce hyphal branching in arbuscular mycorrhizal (AM) fungi. AM fungi form symbioses with higher plant roots and mainly facilitate the absorption of phosphate from the soil. Conforming to the classical definition of a plant hormone, strigolactones are produced in the roots and translocated to the shoots where they inhibit shoot outgrowth and branching. The biosynthesis of this class of compounds is regulated by soil nutrient availability, i.e. the plant will increase its production of strigolactones when the soil phosphate concentration is limited, and decrease production when phosphates are in ample supply. Strigolactones that affect plant shoot branching, AM fungal hyphal branching, and seed ger-mination in parasitic plants facilitate chemical synthesis of similar compounds to control these and other biological processes by exogenous application.     

Overexpression of tomato LeAGP-1 arabinogalactan-protein promotes lateral branching and hampers reproductive development

LeAGP-1 is a glycosylphosphatidylinositol (GPI)-anchored arabinogalactan-protein (AGP) in tomato (Lycopersicon esculentum). Patterns of mRNA expression and protein localization for LeAGP-1 indicate that it likely functions in certain aspects of plant growth and development. To elucidate LeAGP-1 function(s), transgenic tomato plants expressing enhanced green fluorescent protein (GFP) fused to LeAGP-1 [GFP-LeAGP-1] or two LeAGP-1 variants, one lacking the C-terminal GPI-anchor domain [GFP-LeAGP-1DeltaC] and the other lacking the lysine-rich domain [GFP-LeAGP-1DeltaK], under the control of the CaMV35S promoter were produced using Agrobacterium-mediated transformation. Transgenic T0 and T1 lines with high levels of both GFP-LeAGP-1 mRNA and protein: (i) were significantly shorter; (ii) were highly branched; (iii) produced more flower buds, but most of these flowers did not mature, resulting in less fruit production; and (iv) produced seeds that were significantly smaller than normal seeds. Overexpression of LeAGP-1DeltaK had a similar or even more pronounced effect on plant vegetative and reproductive growth, while the effect of LeAGP-1DeltaC overexpression on plant reproduction was minimal. These results indicate that the GPI anchor is critical for LeAGP-1 function. As the phenotype of GFP-LeAGP-1 overexpressing transgenic plants is similar to that of cytokinin-overproducing plants, mRNA expression patterns of LeAGP-1 under different hormone treatments were examined. Cytokinins upregulated LeAGP-1 mRNA expression, while auxins and ABA inhibited LeAGP-1 mRNA expression. Based on these results, GPI-anchored LeAGP-1 most likely functions in plant growth and development in concert with auxin/cytokinin signaling.     

The control of shoot branching: an example of plant information processing

Throughout their life cycle, plants adjust their body plan to suit the environmental conditions in which they are growing. A good example of this is in the regulation of shoot branching. Axillary meristems laid down in each leaf formed from the primary shoot apical meristem can remain dormant, or activate to produce a branch. The decision whether to activate an axillary meristem involves the assessment of a wide range of external environmental, internal physiological and developmental factors. Much of this information is conveyed to the axillary meristem via a network of interacting hormonal signals that can integrate inputs from diverse sources, combining multiple local signals to generate a rich source of systemically transmitted information. Local interpretation of the information provides another layer of control, ensuring that appropriate decisions are made. Rapid progress in molecular biology is uncovering the component parts of this signalling network, and combining this with physiological studies and mathematical modelling will allow the operation of the system to be better understood.     

Activation of tomato PR and wound-related genes by a mutagenized tomato MAP kinase kinase through divergent pathways

A mitogen-activated protein kinase kinase (MAPKK) gene, tMEK2, was isolated from tomato cv. Bonny Best. By mutagenesis, a permanently active variant, tMEK2 ^MUT, was created. Both wild-type tMEK2 and mutant tMEK2 ^MUT were driven by a newly described strong plant constitutive promoter, tCUP, in a tomato protoplast transient gene expression system. Pathogenesis-related genes, PR1b1, PR3 and Twi1, and a wound-inducible gene, ER5, were activated by tMEK2^MUT. Specific inhibitors of p38 class MAPK inhibited tMEK2^MUT-induced activation of PR3 and ER5 genes but not that of the PR1b1 or Twi1 gene. Arabidopsis dual-specificity protein tyrosine phosphatase1 (DsPTP1) and maize protein phosphatase 1 (PP1) inhibited tMEK2^MUT-induced activation of the ER5 gene and the Twi1 gene, respectively, whereas PR1b1 and PR3 were not affected by either AtDsPTP1, or maize PP1, or Arabidopsis protein phosphatase 2A (PP2A). We have demonstrated for the first time that a single MAPKK activates an array of PR and wound-related genes. Our observation indicates that the activation of the genes downstream of tMEK2 occurs through divergent pathways and that tMEK2 may play an important role in the interaction of signal transduction pathways that mediate responses to both biotic (e.g. disease) and abiotic stresses (e.g. wound responsiveness).     

CUC1 gene activates the expression of SAM-related genes to induce adventitious shoot formation

CUP-SHAPED COTYLEDON (CUC)1 encodes members of the NAC family. These are functionally redundant genes that are involved in shoot apical meristem (SAM) formation and cotyledon separation during embryogenesis in Arabidopsis. We analyzed transgenic plants overexpressing CUC1 (35S::CUC1). The cotyledons of these transgenic seedlings regularly had two basal lobes, small and round epidermal cells between the sinuses, and adventitious SAMs on the adaxial surface of this region. This suggests that CUC1 promotes adventitious SAM formation by maintaining epidermal cells in an undifferentiated state. In 35S::CUC1 cotyledons, the class I knotted-like homeobox (KNOX) genes, including SHOOT MERISTEMLESS (STM) and BREVIPEDICELLUS (BP), which are involved in SAM formation and/or maintenance, were ectopically expressed before adventitious SAM formation. In stm mutants, ectopic expression of CUC1 could not induce adventitious SAMs, whereas they continued to be observed in bp mutants. These results suggest that STM, but not BP, is necessary for the formation of adventitious SAMs in 35S::CUC1 cotyledons. Furthermore, we examined the relationship between CUC1 and ASYMMETRIC LEAVES (AS)1 and AS2. The as1 and as2 mutations genetically enhance 35S::CUC1 phenotypes even in the absence of STM function. Interestingly, the as1 mutation can partially rescue the mutant vegetative development phenotypes in the cuc1 cuc2 double mutant. Our results suggest that CUC1 positively regulates SAM formation not only through STM but also through an STM-independent pathway that is negatively regulated by AS1 and AS2.     

Signal integration in the control of shoot branching

Shoot branching is a highly plastic developmental process in which axillary buds are formed in the axil of each leaf and may subsequently be activated to give branches. Three classes of plant hormones, auxins, cytokinins and strigolactones (or strigolactone derivatives) are central to the control of bud activation. These hormones move throughout the plant forming a network of systemic signals. The past decade brought great progress in understanding the mechanisms of shoot branching control. Biological and computational studies have led to the proposal of two models, the auxin transport canalization-based model and the second messenger model, which provide mechanistic explanations for apical dominance.     

Isatin as an auxin source favoring floral and vegetative shoot regeneration from calli produced by thin layer explants of tomato pedicel

Thin layer explants taken from the pedicels and peduncles of flowering tomato plants yielded calli with great organogenetic potential. Of the 15 cultivars tested, 7 regenerated roots, shoots and eventually entire fruit-bearing plants. Calli grown on modified Murashige-Skoog medium responded to varied auxins and cytokinins with different morphogenetic patterns. Thus, naphthaleneacetic acid yielded root-producing calli, while the auxin precursor isatin (indole 2,3-dione) caused the production of calli with vegetative and floral shoots, rarely yielding roots. This may be related to isatin's slow, steady conversion to an active auxin (Plant Physiol 41:1485–1488, 1966) in contrast with naphthaleneacetic acid's immediate presentation of a high level of active auxin. The highest incidence of vegetative shoot (100%) and flower (50%) formation was obtained with 10 M isatin and 3 M zeatin. A few of the flowers developed into ripe fruits. The high frequency of induction of vegetative shoots and flowers before roots with isatin suggests its utility in micropropagation from plant tissue cultures.Abbreviations BAP benzylaminopurine - 2, 4-D 2, 4-dichlorophenoxyacetic acid - GA₃ gibberellic acid - IAA indole-3-acetic acid - IBA indole-3-butyric acid - IPA isopentyladenosine - KN kinetin - NAA naphthaleneacetic acid