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Multiple ER-to-nucleus stress signaling pathways are activated during Plantago asiatica mosaic virus and Turnip mosaic virus infection in Arabidopsis thaliana.
The Plant Journal ( IF 7.2 ) Pub Date : 2020-05-11 , DOI: 10.1111/tpj.14798
Mathieu Gayral 1 , Omar Arias Gaguancela 1 , Evelyn Vasquez 2 , Venura Herath 1, 3, 4 , Francisco J Flores 2, 5 , Martin B Dickman 3 , Jeanmarie Verchot 1, 3
Affiliation  

Pathogens and other adverse environmental conditions can trigger endoplasmic reticulum (ER) stress. ER stress signaling increases the expression of cytoprotective ER‐chaperones. The inositol‐requiring enzyme (IRE1) is one ER stress sensor that is activated to splice the bZIP60 mRNA that produces a truncated transcription factor that activates gene expression in the nucleus. The IRE1/bZIP60 pathway is associated with restricting potyvirus and potexvirus infection. This study shows that the Plantago asiatica mosaic virus (PlAMV) triple gene block 3 (TGB3) and the Turnip mosaic virus (TuMV) 6K2 proteins activate alternative transcription pathways involving the bZIP17, bZIP28, BAG7, NAC089 and NAC103 factors in Arabidopsis thaliana . Using the corresponding knockout mutant lines, we show that bZIP17, bZIP60, BAG7 and NAC089 are factors in reducing PlAMV infection, whereas bZIP28 and bZIP60 are factors in reducing TuMV infection. We propose a model in which bZIP60 and bZIP17 synergistically induce genes restricting PlAMV infection, while bZIP60 and bZIP28 independently induce genes supporting PlAMV infection. Regarding TuMV‐green fluorescent protein (GFP) infection, bZIP60 and bZIP28 serve to repress local and systemic infection. Finally, tauroursodeoxycholic acid treatments were used to demonstrate that the protein folding capacity significantly influences PlAMV accumulation.

中文翻译:

拟南芥中的车前草花叶病毒和芜菁花叶病毒感染过程中激活了多个内质网至细胞核应激信号通路。

病原体和其他不利的环境条件会触发内质网(ER)压力。内质网应激信号增加了细胞保护性内质伴侣的表达。需要肌醇的酶(IRE1)是一种内质网应激传感器,被激活后可以剪接bZIP60 mRNA,从而产生截短的转录因子,从而激活细胞核中的基因表达。IRE1 / bZIP60途径与限制马铃薯痘病毒和马铃薯痘病毒的感染有关。这项研究表明,车前草花叶病毒(PlAMV)三重基因块3(TGB3)和芜菁花叶病毒(TuMV)6K2蛋白激活拟南芥中涉及bZIP17,bZIP28,BAG7,NAC089和NAC103因子的替代转录途径。。使用相应的敲除突变株,我们显示bZIP17,bZIP60,BAG7和NAC089是减少PlAMV感染的因素,而bZIP28和bZIP60是减少TuMV感染的因素。我们提出了一个模型,其中bZIP60和bZIP17协同诱导限制PlAMV感染的基因,而bZIP60和bZIP28独立诱导支持PlAMV感染的基因。关于TuMV绿色荧光蛋白(GFP)感染,bZIP60和bZIP28可抑制局部和全身感染。最后,牛磺去氧胆酸处理用于证明蛋白质折叠能力显着影响P1AMV的积累。
更新日期:2020-05-11
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