拟南芥根中生长素极性运输的研究进展

生长素极性运输影响植物的生长和发育,在植物器官形态建成、发育等过程中发挥重要的调控作用.生长素极性运输是一个依赖于生长素运输载体来完成的复杂过程.近年来生长素极性运输载体AUX/LAX蛋白、PIN蛋白家族和MDR/PGP蛋白家族在生长素极性运输中作用的研究日益深入,并且在植物激素联系和转运方面取得了重大发现——PILC蛋白.     

生长素极性运输研究进展

生长素极性运输与植物生长发育密切相关并受许多因素调控,生长素极性运输机理方面已取得较大进展,但仍有一些亟待解决的问题.研究植物生长素极性运输的生理机制及其调控具有十分重要的意义.通过了解生长素在植物生长发育中的作用,进而阐述生长素极性运输机理方面的研究进展.     

植物生长素的极性运输载体研究进展

生长素极性运输在植物生长发育中起重要的调控作用.植物细胞间的生长素极性运输主要通过生长素运输载体进行调控.该文对近年来有关生长素极性运输载体,包括输入载体AUX/LAX、输出载体PIN、尤其是新近发现的兼有输入和输出载体功能的MDR/PGP等蛋白家族,以及生长素极性运输中PIN与MDR/PGP蛋白间相互作用关系进行综述.     

生长素极性运输研究进展

高等植物的生长发育受激素的广泛调控,其中生长素的作用尤为独特,因为生长素在植物组织内的浓度梯度是由其极性运输维持的,而正是激素在植物组织的相对含量决定了该组织的发育命运。高等植物体内存在可运输的化学信使的概念首先由Ｄａｒｗｉｎ父子提出。通过对金丝鸟木亡草（Ｐｈａｌａｒｉｓｃａ ｎａｒｉｅｎｓｉｓ）幼苗的向光性的研究,他们认为植物的向光性受到一种可运输的物质的调控［1］。后来发现这一物质是生长素,在自然界中主要存在的形式是ＩＡＡ。到本世纪 30年代,禾谷类植物中的生长素的极性运输得到证实,后来发现所有…     

生长素及其运输蛋白对植物铝胁迫的响应

铝对植物的毒害作用主要表现为抑制根尖生长,而根尖生长与生长素及其运输密切相关,铝可能影响了生长素及其代谢过程,但目前尚不清楚生长素及其运输蛋白如何参与植物应对铝胁迫响应。本文通过分析、总结前人研究,并结合自己的前期研究结果,初步阐述生长素或其运输蛋白对植物铝胁迫的响应,即铝影响生长素代谢的相关基因,干扰根尖生长素运输蛋白在细胞内分布及其囊泡运输,调控生长素的极性运榆,进而抑制根尖生长。另一方面,生长素或其运输蛋白又参与了植物应对铝胁迫过程,这主要体现在参与了植物铝毒信号传递、根系铝内置化过程和减缓铝诱导的氧化胁迫。最后,本文提出了生长素及其运输蛋白对植物铝胁迫响应的可能模型。     

生长素在微生物调控根发育过程中的作用

很多微生物通过分泌生长素和生长素前体与植物建立了有益的关系并改变植物根系的形态结构,此外,微生物分泌的其他代谢产物也能改变植物生长素信号通路。因此,生长素和生长素信号通路在微生物调控植物根系发育的过程中起着至关重要的作用。该文从生长素合成、生长素信号和生长素极性运输3个方面总结了生长素在微生物调控植物根系发育过程中的作用,主要包括微生物增加了植物内源生长素的含量、增强了生长素的信号和调控PIN蛋白的表达水平,进而如何调控植物生理和分子水平来适应微生物对其根系的改变,为进一步开展该方面的研究奠定了基础。     

生长素对拟南芥叶片发育调控的研究进展

叶片（包括子叶）是茎端分生组织产生的第一类侧生器官,在植物发育中具有重要地位。早期叶片发育包括三个主要过程：叶原基的起始,叶片腹背性的建立和叶片的延展。大量证据表明叶片发育受到体内遗传机制和体外环境因子的双重调节。植物激素,尤其是生长素在协调体内外调节机制中起着不可或缺的作用。生长素的稳态调控、极性运输和信号转导影响叶片发育的全过程。本文着重介绍生长素在叶片生长发育和形态建成中的调控作用,试图了解复杂叶片发育调控网络。     

植物向重力反应中PIN-FORMED介导的生长素极性运输调控

植物的向性,即植物对光或重力等环境刺激信号产生的定向生长反应。在向重力性反应中,植物器官将重力感知为定向环境信号,来控制其器官的生长方向以促进生存。植物激素生长素及其极性运输在植物向重力反应中起着决定性的调控作用。质膜定位的生长素输出蛋白PIN-FORMED(PIN)通过动态的亚细胞极性定位,改变生长素运输的方向以响应环境刺激,由此植物器官间建立的生长素浓度梯度是细胞差异化伸长和器官弯曲的基础,来调控植物的形态建成和生长发育过程。本文主要讨论发生在植物重力感受细胞内早期重力感知和信号转导机制的最新研究进展、PIN介导的生长素极性运输、PIN的极性定位以及质膜蛋白丰度的调控机制等。     

植物非经典生长素信号转导通路解析

植物激素生长素参与调控植物生长发育的各个过程,包括胚胎发育、器官发生和向性运动等。植物通过协调生长素的合成代谢、极性运输以及信号转导来实现对不同生长发育过程的精准调控。生长素的功能依赖于其信号被感知后经由信号转导通路转换为下游复杂多样的反应。经典的生长素信号转导通路阐明了细胞核内从SCF~(TIR1/AFB)受体到Aux/IAA蛋白的泛素化降解最终通过ARF转录因子调控基因转录的完整生长素响应过程。该核内信号通路揭示了生长素转录调控生长发育的诸多分子机制,但植物生长发育调控过程中仍有许多生长素响应过程无法通过该经典信号通路解析。重点阐述生长素非经典信号通路的调控机制及其对植物生长发育的重要作用,并讨论和展望生长素非经典信号通路研究目前所面临的挑战以及研究前景。     

生长素对拟南芥叶片发育调控的研究进展

叶片(包括子叶)是茎端分生组织产生的第一类侧生器官, 在植物发育中具有重要地位。早期叶片发育包括三个主要过程: 叶原基的起始, 叶片腹背性的建立和叶片的延展。大量证据表明叶片发育受到体内遗传机制和体外环境因子的双重调节。植物激素, 尤其是生长素在协调体内外调节机制中起着不可或缺的作用。生长素的稳态调控、极性运输和信号转导影响叶片发育的全过程。本文着重介绍生长素在叶片生长发育和形态建成中的调控作用, 试图了解复杂叶片发育调控网络。     

Flavonoids act as negative regulators of auxin transport in vivo in arabidopsis

Polar transport of the plant hormone auxin controls many aspects of plant growth and development. A number of synthetic compounds have been shown to block the process of auxin transport by inhibition of the auxin efflux carrier complex. These synthetic auxin transport inhibitors may act by mimicking endogenous molecules. Flavonoids, a class of secondary plant metabolic compounds, have been suggested to be auxin transport inhibitors based on their in vitro activity. The hypothesis that flavonoids regulate auxin transport in vivo was tested in Arabidopsis by comparing wild-type (WT) and transparent testa (tt4) plants with a mutation in the gene encoding the first enzyme in flavonoid biosynthesis, chalcone synthase. In a comparison between tt4 and WT plants, phenotypic differences were observed, including three times as many secondary inflorescence stems, reduced plant height, decreased stem diameter, and increased secondary root development. Growth of WT Arabidopsis plants on naringenin, a biosynthetic precursor to those flavonoids with auxin transport inhibitor activity in vitro, leads to a reduction in root growth and gravitropism, similar to the effects of synthetic auxin transport inhibitors. Analyses of auxin transport in the inflorescence and hypocotyl of independent tt4 alleles indicate that auxin transport is elevated in plants with a tt4 mutation. In hypocotyls of tt4, this elevated transport is reversed when flavonoids are synthesized by growth of plants on the flavonoid precursor, naringenin. These results are consistent with a role for flavonoids as endogenous regulators of auxin transport.     

Flavonoids and Auxin Transport Inhibitors Rescue Symbiotic Nodulation in the Medicago truncatula Cytokinin Perception Mutant cre1

Initiation of symbiotic nodules in legumes requires cytokinin signaling, but its mechanism of action is largely unknown. Here, we tested whether the failure to initiate nodules in the Medicago truncatula cytokinin perception mutant cre1 (cytokinin response1) is due to its altered ability to regulate auxin transport, auxin accumulation, and induction of flavonoids. We found that in the cre1 mutant, symbiotic rhizobia cannot locally alter acro- and basipetal auxin transport during nodule initiation and that these mutants show reduced auxin (indole-3-acetic acid) accumulation and auxin responses compared with the wild type. Quantification of flavonoids, which can act as endogenous auxin transport inhibitors, showed a deficiency in the induction of free naringenin, isoliquiritigenin, quercetin, and hesperetin in cre1 roots compared with wild-type roots 24 h after inoculation with rhizobia. Coinoculation of roots with rhizobia and the flavonoids naringenin, isoliquiritigenin, and kaempferol, or with the synthetic auxin transport inhibitor 2,3,5,-triiodobenzoic acid, rescued nodulation efficiency in cre1 mutants and allowed auxin transport control in response to rhizobia. Our results suggest that CRE1-dependent cytokinin signaling leads to nodule initiation through the regulation of flavonoid accumulation required for local alteration of polar auxin transport and subsequent auxin accumulation in cortical cells during the early stages of nodulation.     

Modulation of P-glycoproteins by auxin transport inhibitors is mediated by interaction with immunophilins

The immunophilin-like FKBP42 TWISTED DWARF1 (TWD1) has been shown to control plant development via the positive modulation of ABCB/P-glycoprotein (PGP)-mediated transport of the plant hormone auxin. TWD1 functionally interacts with two closely related proteins, ABCB1/PGP1 and ABCB19/PGP19/MDR1, both of which exhibit the ability to bind to and be inhibited by the synthetic auxin transport inhibitor N-1-naphylphtalamic acid (NPA). They are also inhibited by flavonoid compounds, which are suspected modulators of auxin transport. The mechanisms by which flavonoids and NPA interfere with auxin efflux components are unclear. We report here the specific disruption of PGP1-TWD1 interaction by NPA and flavonoids using bioluminescence resonance energy transfer with flavonoids functioning as a classical established inhibitor of mammalian and plant PGPs. Accordingly, TWD1 was shown to mediate modulation of PGP1 efflux activity by these auxin transport inhibitors. NPA bound to both PGP1 and TWD1 but was excluded from the PGP1-TWD1 complex expressed in yeast, suggesting a transient mode of action in planta. As a consequence, auxin fluxes and gravitropism in twd1 roots are less affected by NPA treatment, whereas TWD1 gain-of-function promotes root bending. Our data support a novel model for the mode of drug-mediated P-glycoprotein regulation mediated via protein-protein interaction with immunophilin-like TWD1.     

Flavonoids redirect PIN-mediated polar auxin fluxes during root gravitropic responses

The rate, polarity, and symmetry of the flow of the plant hormone auxin are determined by the polar cellular localization of PIN-FORMED (PIN) auxin efflux carriers. Flavonoids, a class of secondary plant metabolites, have been suspected to modulate auxin transport and tropic responses. Nevertheless, the identity of specific flavonoid compounds involved and their molecular function and targets in vivo are essentially unknown. Here we show that the root elongation zone of agravitropic pin2/eir1/wav6/agr1 has an altered pattern and amount of flavonol glycosides. Application of nanomolar concentrations of flavonols to pin2 roots is sufficient to partially restore root gravitropism. By employing a quantitative cell biological approach, we demonstrate that flavonoids partially restore the formation of lateral auxin gradients in the absence of PIN2. Chemical complementation by flavonoids correlates with an asymmetric distribution of the PIN1 protein. pin2 complementation probably does not result from inhibition of auxin efflux, as supply of the auxin transport inhibitor N-1-naphthylphthalamic acid failed to restore pin2 gravitropism. We propose that flavonoids promote asymmetric PIN shifts during gravity stimulation, thus redirecting basipetal auxin streams necessary for root bending.     

Regulation of auxin transport by aminopeptidases and endogenous flavonoids

 The 1-N-naphthylphthalamic acid (NPA)-binding protein is a putative negative regulator of polar auxin transport that has been shown to block auxin efflux from both whole plant tissues and microsomal membrane vesicles. We previously showed that NPA is hydrolyzed by plasma-membrane amidohydrolases that co-localize with tyrosine, proline, and tryptophan-specific aminopeptidases (APs) in the cotyledonary node, hypocotyl-root transition zone and root distal elongation zone of Arabidopsisthaliana (L.) Heynh. seedlings. Moreover, amino acyl-β-naphthylamide (aa-NA) conjugates resembling NPA in structure have NPA-like inhibitory activity on growth, suggesting a possible role of APs in NPA action. Here we report that the same aa-NA conjugates and the AP inhibitor bestatin also block auxin efflux from seedling tissue. Bestatin and, to a lesser extent, some aa-NA conjugates were more effective inhibitors of low-affinity specific [³H]NPA-binding than were the flavonoids quercetin and kaempferol but had no effect on high-affinity binding. Since the APs are inhibited by flavonoids, we compared the localization of endogenous flavonoids and APs in seedling tissue. A correlation between AP and flavonoid localization was found in 5- to 6-d-old seedlings. Evidence that these flavonoids regulate auxin accumulation in vivo was obtained using the flavonoid-deficient mutant, tt4. In whole-seedling [¹⁴C]indole-3-acetic acid transport studies, the pattern of auxin distribution in the tt4 mutant was shown to be altered. The defect appeared to be in auxin accumulation, as a considerable amount of auxin escaped from the roots. Treatment of the tt4 mutant with the missing intermediate naringenin restored normal auxin distribution and accumulation by the root. These results implicate APs and endogenous flavonoids in the regulation of auxin efflux. Received: 2 December 1999 / Accepted: 16 January 2000     

Flavonoids and auxin transport: modulators or regulators?

Flavonoids are polyphenolic compounds found in all vascular and non-vascular plants. Although nonessential for plant growth and development, flavonoids have species-specific roles in nodulation, fertility, defense and UV protection. Flavonoids have been shown to modulate transport of the phytohormone auxin in addition to auxin-dependent tropic responses. However, flavonoids are not essential regulators of these processes because transport and tropic responses occur in their absence. Flavonoids modulate the activity of auxin-transporting P-glycoproteins and seem to modulate the activity of regulatory proteins such as phosphatases and kinases. Phylogenetic analysis suggests that auxin transport mechanisms evolved in the presence of flavonoid compounds produced for the scavenging of reactive oxygen species and defense from herbivores and pathogens.     

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.