The members of the Vicinal oxygen chelate proteins (VOC) superfamily are distributed in both prokaryotic and eukaryotes, and each member has high homology in three-dimensional structure, but the amino acid homology is very low, and the biological function of the protein is still poorly understood. The unfolded protein response (UPR) plays an important role in plant virus infection, but the mechanism by which plant viruses use host proteins to regulate UPR to promote infection is not well understood.
近日，JIPB在线发表了中国农业大学植物保护学院韩成贵/王颖团队题为“A vicinal oxygen chelate protein facilitates viral infection by triggering the unfolded protein response in Nicotiana benthamiana”的研究论文 (https://doi.org/10.1111/jipb.13667)，揭示了VOC1参与正向调控UPR促进植物病毒侵染的分子机制。 本研究以甜菜上重要的丛根病病原甜菜坏死黄脉病毒 (beet necrotic yellow vein virus，BNYVV) 为模型。 研究表明，BNYVV侵染本生烟时诱导VOC1基因的表达，同时激活UPR通路的bZIP17/28分支。 过表达VOC1基因促进BNYVV在本生烟和天然寄主甜菜上的病毒积累，并且该生物学功能依赖VOC1的细胞核定位 (图1)。 通过本生烟转基因超表达、RNAi干扰和基因编辑敲除VOC1植株接种病毒实验，证明VOC1是一个感病基因，能显著地促进BNYVV的侵染。
Figure 1. The susceptibility gene VOC1 promotes BNYVV infection
Further studies proved that VOC1 interacted with bZIP17/28, a transcription factor of UPR pathway, in the nucleus, and enhanced the binding activity of bZIP17/28 to DNA, thereby enhancing the transcriptional activity of BLP4, a downstream gene of UPR activated by bZIP17/28. Overexpression of bZIP17 or bZIP28 genes promoted the viral accumulation of BNYVV on Bunphy Nia, while silencing of endogenous bZIP17 gene in Bunphy Tobacco by VIGS technology reduced the viral accumulation of BNYVV, indicating that the activation of UPR promoted BNYVV infection. At the same time, bZIP17/28 directly binds to the promoter region of VOC1 gene and activates the transcription of VOC1 gene, which promotes the formation of a positive feedback loop of UPR, which is conducive to BNYVV infection of Buntobacco.
This study revealed that VOC1 is a new positive regulator of UPR, and BNYVV utilizes the VOC1-bZIP17/28-UPR module to promote its infection (Fig. 2). These studies deeply analyzed the molecular mechanism of using host proteins to regulate UPR to promote infection in plant viruses, and provided new insights into the role of UPR in the process of plant virus-host interaction. At the same time, the results of this study will expand the understanding of plant susceptibility genes and provide important genetic and theoretical support for the creation of disease resistance breeding materials using gene editing technology.
Figure 2. VOC1-bZIP17/28-UPR is a working model that regulates plant virus infection
Guo Zhihong, a Ph.D. student from the College of Plant Protection, China Agricultural University, and Jiang Ning, a Ph.D. graduate, are the co-first authors of the paper, and Associate Professor Wang Ying from the College of Plant Protection of China Agricultural University is the corresponding author of the paper. Professor Han Chenggui from the College of Plant Protection, China Agricultural University, provided important guidance and assistance for this study. Zhang Zongying, senior experimenter, doctoral students Li Menglin and Liu Qi, and master's students Guo Hongfang and Qin Xinyu participated in the work of the paper. This research was supported by the National Natural Science Foundation of China (32270165 and 31872921) and the National Sugar Modern Agricultural Industry Technology System (CARS-170304). Article Citations:
Guo, Z., Jiang, N., Li, M., Guo, H., Liu, Q., Qin, X., Zhang, Z., Han, C., and Wang, Y. (2024). A vicinal oxygen chelate protein facilitates viral infection by triggering the unfolded protein response in Nicotiana benthamiana. J. Integr. Plant Biol. https://doi.org/10.1111/jipb.13667
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