非TIR1受体依赖型激活生长素信号的新机制

依赖于受体TIR1以及下游Aux/IAAs-ARFs介导的信号通路是目前研究最为深入的生长素信号转导途径。徐通达课题组最新研究发现, 高浓度生长素能够诱导质膜定位的TMK1激酶发生剪切, 导致其羧基(C-)端部分转入细胞核并磷酸化修饰细胞核内的非经典IAA32/34, 后者通过与生长素响应转录因子ARFs互作, 调控下游基因表达, 从而解析了生长素通过TMK1-IAA32/34-ARFs通路调控植物顶端弯钩内外侧差异性生长的分子机制。该研究发现了一条新的生长素TMK1- IAA32/34-ARFs信号途径, 此信号通路独立于经典生长素受体TIR1介导的生长素信号转导通路。     

非TIR1受体依赖型激活生长素信号的新机制

依赖于受体TIR1以及下游Aux/IAAs-ARFs介导的信号通路是目前研究最为深入的生长素信号转导途径。徐通达课题组最新研究发现, 高浓度生长素能够诱导质膜定位的TMK1激酶发生剪切, 导致其羧基(C-)端部分转入细胞核并磷酸化修饰细胞核内的非经典IAA32/34, 后者通过与生长素响应转录因子ARFs互作, 调控下游基因表达, 从而解析了生长素通过TMK1-IAA32/34-ARFs通路调控植物顶端弯钩内外侧差异性生长的分子机制。该研究发现了一条新的生长素TMK1- IAA32/34-ARFs信号途径, 此信号通路独立于经典生长素受体TIR1介导的生长素信号转导通路。     

生长素信号传导研究进展(综述)

近年来,植物激素的信号传导研究已取得突破性进展。本文就生长素的信号传导通路研究,包括生长素应答基因(Aux/IAA),生长素调节因子(ARF)以及感应突变体的研究进行综述。     

生长素信号转导途径与植物胁迫反应相互作用的证据

生长素影响植物多种生理过程,有报道显示生长素可能影响植物对逆境胁迫的反应.我们利用cDNA阵列技术鉴定拟南芥(Arabidopsis thaliana (L.) Heynh.)的生长素应答基因,发现多个胁迫应答基因受生长素抑制,包括Arabidopsis homolog of MEK kinase1 (ATMEKK1),RelA/SpoT homolog 3 (At-RSH3),Catalase 1 (Cat1) 和Ferritin 1 (Fer1),说明生长素可调节胁迫应答基因的表达.此外,我们还证明吲哚乙酸(IAA)合成途径中的腈水解酶基因nitrilase 1 (NIT1) 和nitrilase 2 (NIT2) 受盐胁迫诱导,提示在逆境条件下IAA的合成可能随之增加.我们利用生长素不敏感突变体研究生长素与逆境反应相互作用的信号转导,发现胁迫应答基因在野生型和生长素不敏感突变体auxin resistant 2 (axr2) 中可被盐胁迫诱导,而在auxin resistant 1-3 (axr1-3)中则不被诱导,说明生长素与逆境胁迫反应的相互作用可能发生在泛素途径.     

生长素信号转导途径与植物胁迫反应相互作用的证据(英)

生长素影响植物多种生理过程 ,有报道显示生长素可能影响植物对逆境胁迫的反应。我们利用cDNA阵列技术鉴定拟南芥 (Arabidopsisthaliana (L .)Heynh .)的生长素应答基因 ,发现多个胁迫应答基因受生长素抑制 ,包括ArabidopsishomologofMEKkinase1(ATMEKK1) ,RelA/SpoThomolog 3(At_RSH3) ,Catalase 1(Cat1)和Ferritin 1(Fer1) ,说明生长素可调节胁迫应答基因的表达。此外 ,我们还证明吲哚乙酸 (IAA)合成途径中的腈水解酶基因nitrilase 1(NIT1)和nitrilase 2 (NIT2 )受盐胁迫诱导 ,提示在逆境条件下IAA的合成可能随之增加。我们利用生长素不敏感突变体研究生长素与逆境反应相互作用的信号转导 ,发现胁迫应答基因在野生型和生长素不敏感突变体auxinresistant2 (axr2 )中可被盐胁迫诱导 ,而在auxinresistant1_3(axr1_3)中则不被诱导 ,说明生长素与逆境胁迫反应的相互作用可能发生在泛素途径。     

An Integrative Analysis of the Effects of Auxin on Jasmonic Acid Biosynthesis in Arabidopsis thaliana

Auxin and jasmonic acid （JA） are two plant phytohormones that both participate in the regulation of many developmental processes. Jasmonic acid also plays important roles in plant stress response reactions. Although extensive investigations have been undertaken to study the biological functions of auxin and JA, little attention has been paid to the cross-talk between their regulated pathways. In the few available reports examining the effects of auxin on the expression of JA or JA-responsive genes, both synergetic and antagonistic results have been found. To further investigate the relationship between auxin and JA, we adopted an integrative method that combines microarray expression data with pathway information to study the behavior of the JA biosynthesis pathway under auxin treatment. Our results showed an overall downregulation of genes involved in JA biosynthesis, providing the first report of a relationship between auxin and the JA synthesis pathway in Arabidopsis seedlings.     

Suppression of auxin signalling promotes rice susceptibility to Rice black streaked dwarf virus infection

Auxin plays a fundamental role in plant growth and development, and also influences plant defence against various pathogens. Previous studies have examined the different roles of the auxin pathway during infection by biotrophic bacteria and necrotrophic fungi. We now show that the auxin signalling pathway was markedly down-regulated following infection of rice by Rice black streaked dwarf virus (RBSDV), a dsRNA virus. Repression of the auxin receptor TIR1 by a mutant overexpressing miR393 increased rice susceptibility to RBSDV. Mutants overexpressing the auxin signalling repressors OsIAA20 and OsIAA31 were also more susceptible to RBSDV. The induction of jasmonic acid (JA) pathway genes in response to RBSDV was supressed in auxin signalling mutants, suggesting that activation of the JA pathway may be part of the auxin signalling-mediated rice defence against RBSDV. More importantly, our results also revealed that OsRboh-mediated reactive oxygen species levels played important roles in this defence. The results offer novel insights into the regulatory mechanisms of auxin signalling in the rice–RBSDV interaction.     

油菜素甾醇类与生长素的相互作用

油菜素甾醇类(brassinosteroid,BR)和生长素是两类重要的植物激素,二者在许多生理功能上存在相关性。近年来的研究表明,BR与生长素能协同调节基因表达,二者在代谢、运输和信号转导途径等不同层次上存在相互作用,并且这两种信号与其他信号转导途径,如激素信号转导途径和光信号转导途径之间也存在信号对话。现对BR与生长素之间这种复杂的相互作用进行评述。     

Auxin receptors: recent developments

Rapid advances have been made in the study of auxin binding proteins (ABPs) in the last five years. In particular, an ABP in maize membranes has been cloned, sequenced and both monoclonal and polyclonal antibodies to this ABP have been developed. Structural and functional analysis has begun and there is good electrophysiological evidence that ABP in the plasma membrane functions as a receptor, probably involved in auxin-induced cell expansion. The role of the large amount of ABP in the endoplasmic reticulum is less clear, as is the relationship to soluble ABPs. At present there is only some circumstantial evidence relating any ABP to cell division. Receptors for synthetic inhibitors of auxin transport (phytotropins) are also of interest in relation to auxin action, but are less well characterised. Identification of new naturally-occurring phytotropins could lead to novel plant growth regulators.     

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。     

Polar auxin transport – old questions and new concepts?

Polar auxin transport controls multiple aspects of plant development including differential growth, embryo and root patterning and vascular tissue differentiation. Identification of proteins involved in this process and availability of new tools enabling `visualization' of auxin and auxin routes in planta largely contributed to the significant progress that has recently been made. New data support classical concepts, but several recent findings are likely to challenge our view on the mechanism of auxin transport. The aim of this review is to provide a comprehensive overview of the polar auxin transport field. It starts with classical models resulting from physiological studies, describes the genetic contributions and discusses the molecular basis of auxin influx and efflux. Finally, selected questions are presented in the context of developmental biology, integrating available data from different fields.     

A small molecule with differential effects on the PTS1 and PTS2 peroxisome matrix import pathways

The use of small molecules has great power to dissect biological processes. This study presents the identification and characterisation of an inhibitor of peroxisome matrix protein import. A mini-screen was carried out to identify molecules that cause alteration in peroxisome morphology, or mislocalization of a peroxisome targeted fluorescent reporter protein. A benzimidazole lead compound (LDS-003655) was identified that resulted in reduced GFP fluorescence in peroxisomes and cytosolic GFP accumulation. The effect of the compound was specific to peroxisomes as Golgi bodies, endoplasmic reticulum and the actin cytoskeleton were unaffected even at 25 μM, whereas peroxisome import via the PTS1 pathway was compromised at 100 nM. When seedlings were grown on 25 μM LDS-003655 they displayed morphology typical of seedlings grown in the presence of auxin, and expression of the auxin reporter DR5::GFP was induced. Analysis of a focussed library of LDS-003655 derivatives in comparison with known auxins led to the conclusion that the auxin-like activity of LDS-003655 is attributable to its in situ hydrolysis giving rise to 2,5-dichlorobenzoic acid, whereas the import inhibiting activity of LDS-003655 requires the whole molecule. None of the auxins tested had any effect on peroxisome protein import. Matrix import by the PTS2 import pathway was relatively insensitive to LDS-003655 and its active analogues, with effects only seen after prolonged incubation on high concentrations. Steady-state protein levels of PEX5, the PTS1 import pathway receptor, were reduced in the presence of 100 nM LDS-003655, suggesting a possible mechanism for the import inhibition.