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Cucumber Mosaic Virus Movement Protein Severs Actin Filaments to Increase the Plasmodesmal Size Exclusion Limit in Tobacco

机译:黄瓜花叶病毒移动​​蛋白切断肌动蛋白丝增加烟草的血浆大小排阻极限

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摘要

Plant viral movement proteins (MPs) enable viruses to pass through cell walls by increasing the size exclusion limit (SEL) of plasmodesmata (PD). Here, we report that the ability of Cucumber mosaic virus (CMV) MP to increase the SEL of the PD could be inhibited by treatment with the actin filament (F-actin)–stabilizing agent phalloidin but not by treatment with the F-actin–destabilizing agent latrunculin A. In vitro studies showed that CMV MP bound globular and F-actin, inhibited actin polymerization, severed F-actin, and participated in plus end capping of F-actin. Analyses of two CMV MP mutants, one with and one without F-actin severing activities, demonstrated that the F-actin severing ability was required to increase the PD SEL. Furthermore, the Tobacco mosaic virus MP also exhibited F-actin severing activity, and its ability to increase the PD SEL was inhibited by treatment with phalloidin. Our data provide evidence to support the hypothesis that F-actin severing is required for MP-induced increase in the SEL of PD. This may have broad implications in the study of the mechanisms of actin dynamics that regulate cell-to-cell transport of viral and endogenous proteins.
机译:植物病毒移动蛋白(MPs)使病毒通过增加质粒(PD)的尺寸排阻极限(SEL)来穿过细胞壁。在这里,我们报道黄瓜花叶病毒(CMV)MP增加PD SEL的能力可能受到肌动蛋白丝(F-actin)稳定剂鬼笔环肽治疗的抑制,而不受F-actin的治疗所抑制。体外研究表明,CMV MP结合球状蛋白和F-肌动蛋白,抑制肌动蛋白聚合,切断F-肌动蛋白,并参与了F-肌动蛋白的正封端。对两个CMV MP突变体(一个具有和不具有F-肌动蛋白切断活性)的分析表明,需要F-肌动蛋白切断能力来增加PD SEL。此外,烟草花叶病毒MP还表现出F-肌动蛋白切断活性,并且通过用鬼笔环肽处理抑制了其增加PD SEL的能力。我们的数据提供了证据支持MP诱导PD SEL升高需要F-actin切断的假说。这可能在肌动蛋白动力学调节病毒和内源蛋白的细胞间运输机制的研究中具有广泛的意义。

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