The IRE1/bZIP60 Pathway and Bax Inhibitor 1 Suppress Systemic Accumulation of Potyviruses and Potexviruses in Arabidopsis and Nicotiana benthamiana Plants
The IRE1/bZIP60 Pathway and Bax Inhibitor 1 Suppress Systemic Accumulation of Potyviruses and Potexviruses in Arabidopsis and Nicotiana benthamiana Plants
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DOI：
10.1094/mpmi-07-16-0147-r
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发表时间：
2016-10-01
影响因子：
3.5
通讯作者：
Verchot, Jeanmarie
中科院分区：
文献类型：
--
作者：
Gaguancela, Omar Arias;Zuniga, Lizbeth Pena;Verchot, Jeanmarie
肌醇需要酶（IRE 1）是内质网（ER）应激传感器。当被激活时，它剪接bZIP 60 mRNA，产生一个截短的转录因子，上调参与未折叠蛋白反应的基因。Bax抑制剂1（BI-1）是另一种ER应激传感器，其调节细胞响应环境攻击的死亡。已知马铃薯Y病毒6 K2和马铃薯X病毒TGB 3蛋白存在于ER中，分别作为病毒复制酶和运动蛋白复合物的锚。本研究使用绿色荧光蛋白（GFP）标记的芜菁花叶病毒（TuMV）、车前草花叶病毒（PIAMV）、马铃薯病毒Y（PVY）和马铃薯病毒X（PVX）来确定IRE 1/bZIP 60途径和BI-1机制在拟南芥、本氏烟草和马铃薯中的病毒感染早期被诱导。仅将马铃薯Y病毒6 K2或TGB 3基因农杆菌介导到植物细胞中激活了拟南芥（Arabidopsis thaliana）、N. benthamiana和S.马铃薯用TuMV-GFP或PlAMV-GFP接种纯合ire 1a-2、ire 1b-4和ire 1a-2/ire 1b-4突变体拟南芥植物。PIAMV在ire 1a-2或ire 1a-2/ire 1b-4突变体植物中的积累水平高于ire 1b-4或野生型植物。与野生型植物相比，TuMV-GFP在ire 1a-2、ire 1b-4或ire 1a-2/ire 1b-4中积累到更高的水平，这表明两种同种型都有助于TuMV-GFP感染。基因沉默用于敲低N.本萨米亚纳与对照植物相比，PVX-GFP和PVY-GFP积累在这些沉默植物中显著升高。这项研究表明，两个ER应激途径，即IRE 1/bZIP 60和BI-1途径，限制了马铃薯Y病毒和马铃薯X病毒感染的系统积累。沉默BI-1表达也导致全身性坏死。这些数据表明，由IRE 1和BI-1领导的ER应激激活途径响应于入侵的马铃薯Y病毒属和马铃薯X病毒属，以限制病毒感染并使生理变化能够使植物耐受病毒攻击。
The inositol requiring enzyme (IRE1) is an endoplasmic reticulum (ER) stress sensor. When activated, it splices the bZIP60 mRNA, producing a truncated transcription factor that upregulates genes involved in the unfolded protein response. Bax inhibitor 1 (BI-1) is another ER stress sensor that regulates cell death in response to environmental assaults. The potyvirus 6K2 and potexvirus TGB3 proteins are known to reside in the ER, serving, respectively, as anchors for the viral replicase and movement protein complex. This study used green fluorescent protein (GFP)-tagged Turnip mosaic virus (TuMV), Plantago asiatica mosaic virus (PIAMV), Potato virus Y (PVY), and Potato virus X (PVX) to determine that the IRE1/bZIP60 pathway and BI-1 machinery are induced early in virus infection in Arabidopsis thaliana, Nicotiana benthamiana, and Solanum tuberosum. Agrodelivery of only the potyvirus 6K2 or TGB3 genes into plant cells activated bZIP60 and BI-1 expression in Arabidopsis thaliana, N. benthamiana, and S. tuberosum. Homozygous ire1a-2, ire1b-4, and ire1a-2/ire1b-4 mutant Arabidopsis plants were inoculated with TuMV-GFP or PlAMV-GFP. PIAMV accumulates to a higher level in ire1a-2 or ire1a-2/ire1b-4 mutant plants than in ire1b-4 or wild-type plants. TuMV-GFP accumulates to a higher level in ire1a-2, ire1b-4, or ire1a-2/ire1b-4 compared with wild-type plants, suggesting that both isoforms contribute to TuMV-GFP infection. Gene silencing was used to knock down bZIP60 and BI-1 expression in N. benthamiana. PVX-GFP and PVY-GFP accumulation was significantly elevated in these silenced plants compared with control plants. This study demonstrates that two ER stress pathways, namely IRE1/bZIP60 and the BI-1 pathway, limit systemic accumulation of potyvirus and potexvirus infection. Silencing BI-1 expression also resulted in systemic necrosis. These data suggest that ER stress activated pathways, led by IRE1 and BI-1, respond to invading potyvirus and potexviruses to restrict virus infection and enable physiological changes enabling plants to tolerate virus assault.