Transcription factor ANAC032 modulates JA/SA signalling in response to Pseudomonas syringae infection

Transcription factor ANAC032 modulates JA/SA signalling in response to Pseudomonas syringae infection
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DOI:
10.15252/embr.201642197
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发表时间:
2016-11-01
期刊:
影响因子:
7.7
通讯作者:
Balazadeh, Salma
Balazadeh, Salma
中科院分区:
生物学2区
文献类型:
--
作者:
Allu, Annapurna Devi;Brotman, Yariv;Balazadeh, Salma

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对病原体的反应,包括宿主转录重编程,需要依赖于植物激素水杨酸(SA)和茉莉酸(JA)的部分拮抗信号通路。然而,上游因素调节这些途径的相互作用没有得到很好的表征。在这里,我们确定了转录因子ANAC032从拟南芥作为一个这样的调节器在响应细菌病原体假单胞菌pv。番茄DC3000(Pst.)ANAC032在Pst攻击时直接抑制MYC2活化,导致冠菌素介导的气孔重新打开的阻断,从而限制细菌进入植物组织。此外,ANAC032通过抑制NIMIN 1激活SA信号传导,NIMIN 1是SA依赖性防御的关键负调节因子。最后,ANAC032减少JA反应基因的表达,包括PDF1.2A。因此,ANAC032通过产生针对通过ANAC032与MYC2、NIMIN1和PDF1.2A启动子的直接结合协调的关键SA和JA信号传导基因的协调转录输出来增强对Pst的抗性。
Responses to pathogens, including host transcriptional reprogramming, require partially antagonistic signalling pathways dependent on the phytohormones salicylic (SA) and jasmonic (JA) acids. However, upstream factors modulating the interplay of these pathways are not well characterized. Here, we identify the transcription factor ANAC032 from Arabidopsis thaliana as one such regulator in response to the bacterial pathogen Pseudomonas syringae pv. tomato DC3000 (Pst). ANAC032 directly represses MYC2 activation upon Pst attack, resulting in blockage of coronatine-mediated stomatal reopening which restricts entry of bacteria into plant tissue. Furthermore, ANAC032 activates SA signalling by repressing NIMIN1, a key negative regulator of SA-dependent defence. Finally, ANAC032 reduces expression of JA-responsive genes, including PDF1.2A. Thus, ANAC032 enhances resistance to Pst by generating an orchestrated transcriptional output towards key SA- and JA-signalling genes coordinated through direct binding of ANAC032 to the MYC2, NIMIN1 and PDF1.2A promoters.