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    植物病毒侵染诱导寄主内质网应激反应

    Endoplasmic Reticulum Stress Induced by Plant Viral Infection

    • 摘要: 病毒侵染产生的大量病毒蛋白阻碍细胞转运功能,未折叠或错折叠蛋白在内质网腔蓄积导致内质网应激(ERs),诱发细胞保护信号未折叠蛋白应答(UPR),或导致细胞程序性死亡(PCD)。在明确了动物病毒诱导的ERs相关的UPR信号通路基础上,从非生物因素诱导的拟南芥ERs应答信号和植物病毒侵染引起ERs两方面,对近年的研究成果进行了概述。归纳出植物病毒侵染诱导寄主ERs,包括改变ER膜形态和激活UPR基因。分析了ERs应答信号在病毒侵染过程中的重要作用,指出病毒调控UPR通路完成侵染复制,寄主则通过PCD通路以主动消亡的方式抵御病毒。但UPR和PCD的关系尚不明晰,不同的病毒调控UPR信号的机制及信号强弱尚不明确,寻找病毒诱发寄主UPR和逃避寄主PCD建立侵染关系的关键调节子,是抗病毒研究的发展方向。

       

      Abstract: The cellular translation machinery is hijacked by large amounts of viral proteins upon viral infection. As a result, the unfolded or misfolded proteins accumulated in the lumen of the endoplasmic reticulum leads to ER stress (ERs), which triggers the unfolded protein response (UPR) or programmed cell death (PCD). On the basis of the ERs-related UPR signaling induced by animal viruses, this review summarizes recent understanding of the ERs signaling induced by abiotic factors in Arabidopsis and triggered by plant viral infection, reviews the ERs induced in plant virus infected cell, including the morphological changes of ER membranes and the activation of UPR genes, analyzes the vital role of ERs signaling in viral infection, and points out that the viruses manipulate UPR in favor of their replication and the host initiates PCD of apoptosis to resist viruses. Little is known about the crosstalk between different UPR arms and PCD, and signal strength of UPR regulated by different viruses. Searching for the key regulators of virus induced host UPR and escaped from host PCD is the developing direction of antiviral research.

       

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