Arabidopsis GH3.5 regulates salicylic acid-dependent and both NPR1-dependent and independent defense responses

Arabidopsis GH3.5 regulates salicylic acid-dependent and both NPR1-dependent and independent defense responses
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拟南芥 GH3.5 调节水杨酸依赖性以及 NPR1 依赖性和独立防御反应

DOI:
10.4161/psb.3.8.5748
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发表时间:
2008-04
影响因子:
2.9
通讯作者:
Muyang Wang
Muyang Wang
中科院分区:
生物学4区
文献类型:
--
作者:
Zuhua He;Zhimiao Li;Qun Li;Zhongqin Zhang;Muyang Wang

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植物抗病性和发育之间的相互作用是理解病原体侵袭过程中系统生理过程的基础。我们的前期研究表明,拟南芥GH3.5基因在拟南芥-假单胞菌互作和发育过程中,对水杨酸(SA)介导的抗性和生长素介导的敏感性起着双功能调节剂的作用。本文进一步研究了GH3.5在SA依赖性防御途径中的作用和机制。GH3.5启动子::GUS报告基因表达的转录和组织化学分析表明,GH3.5以强的时间和空间方式表达,主要在分裂组织中表达。在细菌攻击后,GUS活性在浸润区周围的接合组织中被诱导,在脉管系统中具有更高的水平,在不相容和相容相互作用之间具有不同的模式。外源SA的施用增强了激活标记突变体gh3.5-1D的抗病性,而GH3.5介导的防御增强在SA缺陷型gh3.5-1D/NahG双突变体中被耗尽,表明GH3.5通过SA依赖的途径调节防御反应。此外,细菌生长的gh3.5-1D/npr 1双突变体处理SA表明,GH3.5增强SA介导的防御反应,通过NPR 1依赖和独立的途径。
The cross-talk between plant disease resistance and development is fundamental to understanding systemic physiological processes during pathogen attack. Our previous study showed that the Arabidopsis GH3.5 gene acts as a bifunctional modulator of the salicylic acid (SA)-mediated resistance and the auxin-mediated susceptibility during the Arabidopsis-Pseudomonas syringae interaction as well as development. Here, we further study the role and mechanism of GH3.5 involved in the SA-dependent defense pathway. Transcript and histochemical analysis of the GH3.5 promoter::GUS reporter expression indicate that GH3.5 is expressed with a strong temporal and spatial manner with predominant expression in the divisional tissues. Upon bacterial challenge, GUS activity is induced in the junction tissue around the infiltrated zone with higher levels in the vasculature with a pattern different between the incompatible and compatible interactions. Exogenous SA application enhances disease resistance in the activation-tagged mutant gh3.5-1D, while the GH3.5-mediated defense enhancement is depleted in the SA deficient gh3.5-1D/NahG double mutant, indicating that GH3.5 modulates defense response through the SA-dependent pathway. Furthermore, bacterial growth in the gh3.5-1D/npr1 double mutant treated with SA indicates that GH3.5 enhances the SA-mediated defense response through both NPR1-dependent and independent pathways.
DOI: 10.1371/journal.ppat.0020123
发表时间: 2006-11
期刊: PLOS PATHOGENS
影响因子: 6.7
作者:
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DOI: 10.1126/science.266.5188.1247
发表时间: 1994-11-18
期刊: SCIENCE
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发表时间: 2007-12-11
影响因子: 11.1
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通讯作者: Kunkel, Barbara N.
DOI: 10.1016/s1534-5807(04)00028-0
发表时间: 2004-02-01
期刊: DEVELOPMENTAL CELL
影响因子: 11.8
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发表时间: 2001-11-29
期刊: NATURE
影响因子: 64.8
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