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Ferredoxin 1 is downregulated by the accumulation of abscisic acid in an ABI5‐dependent manner to facilitate rice stripe virus infection in Nicotiana benthamiana and rice

生物 马铃薯卷叶病毒 烟草 基因沉默 脱落酸 基因 细胞生物学 病毒学 病毒 植物病毒 遗传学
作者
Weijun Cui,Shu Wang,Kelei Han,Ersong Zheng,Mengfei Ji,Binghua Chen,Xüming Wang,Jianping Chen,Fei Yan
出处
期刊:Plant Journal [Wiley]
卷期号:107 (4): 1183-1197 被引量:23
标识
DOI:10.1111/tpj.15377
摘要

Ferredoxin 1 (FD1) accepts and distributes electrons in the electron transfer chain of plants. Its expression is universally downregulated by viruses and its roles in plant immunity have been brought into focus over the past decade. However, the mechanism by which viruses regulate FD1 remains to be defined. In a previous report, we found that the expression of Nicotiana benthamiana FD1 (NbFD1) was downregulated following infection with potato virus X (PVX) and that NbFD1 regulates callose deposition at plasmodesmata to play a role in defense against PVX infection. We now report that NbFD1 is downregulated by rice stripe virus (RSV) infection and that silencing of NbFD1 also facilitates RSV infection, while viral infection was inhibited in a transgenic line overexpressing NbFD1, indicating that NbFD1 also functions in defense against RSV infection. Next, a RSV-derived small interfering RNA was identified that contributes to the downregulation of FD1 transcripts. Further analysis showed that the abscisic acid (ABA) which accumulates in RSV-infected plants also represses NbFD1 transcription. It does this by stimulating expression of ABA insensitive 5 (ABI5), which binds the ABA response element motifs in the NbFD1 promoter, resulting in negative regulation. Regulation of FD1 by ABA was also confirmed in RSV-infected plants of the natural host rice. The results therefore suggest a mechanism by which virus regulates chloroplast-related genes to suppress their defense roles.

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