检索结果-南通市图书馆

Antagonism of Transcription Factor MYC2 by EDS1/PAD4 Complexes Bolsters Salicylic Acid Defense in Arabidopsis Effector-Triggered Immunity

引用

Molecular Plant 2018年第8期11卷 1053-1066页

作者： Haitao Cui Jingde Qiu Yue Zhou Deepak D. Bhandari Chunhui Zhao Jaqueline Bautor jane E. parker Department of Plant-Microbe Interactions Max-Planck Institute for Plant Breeding Research Carl-von-Linne Weg 10 50829 Cologne Germany Department of Plant Developmental Biology Max-Planck Institute for Plant Breeding Research 50829 Cologne Germany Key Laboratory of Ministry of Education for Genetics Breeding and Multiple Utilization of Crops Plant Immunity Center Fujian Agriculture University Fuzhou 350002 China These authors contributed equaily to this article.

In plant immunity, pathogen-activated intracellular nucleotide binding/leucine rich repeat （NLR） receptors mobilize disease resistance pathways, but the downstream signaling mechanisms remain obscure. Enhanced disease susceptibility 1 （EDS1） controls transcriptional reprogramming in resistance triggered by Toll-lnterleukinl-Receptor domain （TIR）-family NLRs （TNLs）. Transcriptional induction of the salicylic acid （SA） hormone defense sector provides one crucial barrier against biotrophic pathogens. Here, we present genetic and molecular evidence that in Arabidopsis an EDS1 complex with its partner PAD4 inhibits MYC2, a master regulator of SA-antagonizing jasmonic acid （JA） hormone pathways. In the TNL immune response, EDSl/PAD4 interference with MYC2 boosts the SA defense sector independently of EDS1-induced SA synthesis, thereby effectively blocking actions of a potent bacterial JA mimic, coronatine （COR）. We show that antagonism of MYC2 occurs after COR has been sensed inside the nucleus but before or coincident with MYC2 binding to a target promoter, pANAC019. The stable interaction of PAD4 with MYC2 in planta is competed by EDS1-PAD4 complexes. However, suppression of MYC2-promoted genes requires EDS1 together with PAD4, pointing to an essential EDS1-PAD4 heterodimer activity in MYC2 inhibition. Taken together, these results uncover an immune receptor signaling circuit that intersects with hormone pathway crosstalk to reduce bacterial pathogen growth.

关键词： NLR receptor stress hormone network Pseudomonas syringae AvrRps4 RRS1/RPS4 coi1

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Repression of the Auxin Response Pathway Increases Arabidopsis Susceptibility to Necrotrophic Fungi

引用

Molecular Plant 2008年第3期1卷 496-509页

作者： Francisco Llorente Paul M usksktt Andrea Sanchez-Vallet Gemma Lopez Brisa Ramos Clara Sanchez-Rodriguez Lucia Jorda jane parker Antonio Molina Centro de Biotecnologia y Genbmica de Plantas (CBGP) Departamento de Biotecnologia-UPM ETS Ingenieros Agrbnomos Avda Complutense E-28040Madrid Spain Department of Plant-Microbe Interactions Max Planck Institute for Plant Breeding Research Carl-von-Linne Weg 10 50829 Cologne Germany

In plants, resistance to necrotrophic pathogens depends on the interplay between different hormone systems, such as those regulated by salicylic acid （SA）, jasmonic acid （JA）, ethylene, and abscisic acid. Repression of auxin signaling by the SA pathway was recently shown to contribute to antibacterial resistance. Here, we demonstrate that Arabidopsis auxin signaling mutants axrl, axr2, and axr6 that have defects in the auxin-stimulated SCF （Skpl-Cullin- F-box） ubiquitination pathway exhibit increased susceptibility to the necrotrophic fungi Plectosphaerella cucumerina and Botrytis cinerea. Also, stabilization of the auxin transcriptional repressor AXR3 that is normally targeted for removal by the SCF-ubiquitin/proteasome machinery occurs upon P. cucumerina infection. Pharmacological inhibition of auxin transport or proteasome function each compromise necrotroph resistance of wild-type plants to a similar extent as in non-treated auxin response mutants. These results suggest that auxin signaling is important for resistance to the necrotro- phic fungi P. cucumerina and B. cinerea. SGTlb （one of two Arabidopsis SGT1 genes encoding HSP90/HSC70 co-chaperones） promotes the functions of SCF E3-ubiquitin ligase complexes in auxin and JA responses and resistance conditioned by certain Resistance （R） genes to biotrophic pathogens. We find that sgtlb mutants are as resistant to P. cucumerina as wild-type plants. Conversely, auxin/SCF signaling mutants are uncompromised in RPP4-triggered resistance to the obligate biotrophic oomycete, Hyaloperonospora parasitica. Thus, the predominant action of SGTlb in R gene-conditioned resis- tance to oomycetes appears to be at a site other than assisting SCF E3-ubiquitin ligases. However, genetic additivity of sgtlb axrl double mutants in susceptibility to H. parasitica suggests that SCF-mediated ubiquitination contributes to lim- iting biotrophic pathogen colonization once plant-pathogen compatibility is established.

关键词： plant defense innate immunity necrotrophic fungi auxin signaling proteasome.

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Roles of Arabidopsis Patatin-Related Phospholipases A in Root Development Are Related to Auxin Responses and Phosphate Deficiency

引用

Molecular Plant 2010年第3期3卷 524-538页

作者： Steffen Rietz Georgi Dermendjiev Esther Oppermann Fikadu Getah Tafesse Yunus Effendi Andre Holk jane E. parker Markus Teige Gunther F.E. Scherer Max Planck Institute for Plant Breeding Research Department of Plant Microbe Interactions Carl von Linne Weg 10 D-50829 Cologne Germany Leibniz University Hannover Molecular Developmental Physiology Herrenhauser Str. 2 D-30419 Hannover Germany University of Vienna MFPL Department of Biochemistry Dr. Bohrgasse 9 A-1030 Wien Austria Present address: University of Utrecht Department of Membrane Enzymology Inst. Biomembranes Padualaan 8 NL 3584 CH Utrecht. The Netherlands

Phospholipase A enzymes cleave phospho- and galactolipids to generate free fatty acids and lysolipids that function in animal and plant hormone signaling. Here, we describe three Arabidopsis patatin-related phospholipase A （pPLA） genes AtPLAIVA, AtPLAIVB, and AtPLAIVC and their corresponding proteins. Loss-of-function mutants reveal roles for these pPLAs in roots during normal development and under phosphate deprivation. AtPLAIVA is expressed strongly and exclusively in roots and AtplalVA-null mutants have reduced lateral root development, characteristic of an impaired auxin response. By contrast, AtPLAIVB is expressed weakly in roots, cotyledons, and leaves but is transcriptionally induced by auxin, although AtplalVB mutants develop normally. AtPLAIVC is expressed in the floral gynaecium and is induced by abscisic acid （ABA） or phosphate deficiency in roots. While an AtplalVC-1 loss-of-function mutant displays ABA respon- siveness, it exhibits an impaired response to phosphate deficiency during root development. Recombinant AtPLA proteins hydrolyze preferentially galactolipids and, less efficiently, phospholipids, although these enzymes are not localized in chloroplasts. We find that AtPLAIVA and AtPLAIVB are phosphorylated by calcium-dependent protein kinases in vitro and this enhances their activities on phosphatidylcholine but not on phosphatidylglycerol. Taken together, the data reveal novel functions of pPLAs in root development with individual roles at the interface between phosphate deficiency and auxin signaling.

关键词： Abiotic/environmental stress hormonal regulation protein phosphorylation/dephosphorylation signaltransduction gene regulation Arabidopsis.

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

植物抗病的分子机理研究

引用

国外科技新书评介 2009年第9期 16-17页

作者： jane parker Wiley -Blackwell 杨红娟 Max-Planek Institute of PlantBreeding Research Cologne Germany 不详中国科学院植物研究所

植物生长在自然环境中一般能健康成长，由于各种原因有些植物也可能会染病而出现斑点和叶片卷曲现象，但绝大多数植物都能产生抗性并能正常繁衍下一代。这种生存能力得益于植物高效的免疫系统，它能保护它的每个细胞免于被病害和虫害侵... 详细信息

植物生长在自然环境中一般能健康成长，由于各种原因有些植物也可能会染病而出现斑点和叶片卷曲现象，但绝大多数植物都能产生抗性并能正常繁衍下一代。这种生存能力得益于植物高效的免疫系统，它能保护它的每个细胞免于被病害和虫害侵染。只有寄生株系能穿越植物的层层天然防御系统而让植物染病。

关键词：植物抗病分子机理自然环境植物生长免疫系统防御系统繁衍抗性

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：