Tubule-guided cell-to-cell movement of a plant virus requires class XI myosin motors.
Tubule-guided cell-to-cell movement of a plant virus requires class XI myosin motors.
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DOI：
10.1371/journal.ppat.1002327
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发表时间：
2011-10
期刊：
影响因子：
6.7
通讯作者：
Ritzenthaler C
中科院分区：
文献类型：
--
作者：
Amari K;Lerich A;Schmitt-Keichinger C;Dolja VV;Ritzenthaler C
植物病毒的细胞间运动是通过胞间连丝（PD）进行的，胞间连丝是一种进化为促进细胞间通讯的细胞器。病毒运动蛋白 (MP) 会修饰 PD，以允许病毒颗粒或核蛋白通过。该通道通过几种不同的机制发生，其中之一是MP依赖性小管的形成，该小管穿过PD并为病毒体易位提供管道。包括葡萄扇叶病毒 (GFLV) 在内的小管形成病毒的 MP 会募集称为胞连丝定位蛋白 (PDLP) 的植物 PD 受体来介导小管组装和病毒运动。在这里，我们表明 PDLP1 以肌球蛋白依赖性方式通过分泌途径内的特定途径转运至 PD。这种运输主要依赖于 XI 类肌球蛋白 XI-K 和 XI-2。使用显性失活抑制使这些肌球蛋白失活，导致 PDLP 和 MP 的错误定位以及 GFLV 运动的抑制。我们还发现，高尔基体、质膜、PD、质膜内脂筏子结构域和液泡膜的特定标记的正确靶向不受肌球蛋白 XI-K 抑制的影响。然而，正常的液泡膜动力学需要肌球蛋白 XI-K 活性。这些结果揭示了肌球蛋白依赖性蛋白质向 PD 运输的新途径，该途径被 GFLV 劫持，以促进该病毒在植物细胞之间的小管引导运输。为了建立感染，植物病毒通过细胞壁胞间连丝 (PD) 中的狭窄通道在细胞间传播。运动蛋白 (MP) 是病毒编码的蛋白，对于病毒通过 PD 进行细胞间运输至关重要。胞间连丝定位的植物蛋白 (PDLP) 可以被小管形成病毒的 MP 特异性识别。在这里，我们表明 PDLP 靶向 PD 取决于分子马达肌球蛋白 XI-K 和 XI-2。一致地，为了支持 PDLP 作为 MP 的 PD 受体的功能，显性失活肌球蛋白突变体的过度表达抑制葡萄扇叶病毒 (GFLV) MP 的小管形成，并显着减少病毒运动。
Cell-to-cell movement of plant viruses occurs via plasmodesmata (PD), organelles that evolved to facilitate intercellular communications. Viral movement proteins (MP) modify PD to allow passage of the virus particles or nucleoproteins. This passage occurs via several distinct mechanisms one of which is MP-dependent formation of the tubules that traverse PD and provide a conduit for virion translocation. The MP of tubule-forming viruses including Grapevine fanleaf virus (GFLV) recruit the plant PD receptors called Plasmodesmata Located Proteins (PDLP) to mediate tubule assembly and virus movement. Here we show that PDLP1 is transported to PD through a specific route within the secretory pathway in a myosin-dependent manner. This transport relies primarily on the class XI myosins XI-K and XI-2. Inactivation of these myosins using dominant negative inhibition results in mislocalization of PDLP and MP and suppression of GFLV movement. We also found that the proper targeting of specific markers of the Golgi apparatus, the plasma membrane, PD, lipid raft subdomains within the plasma membrane, and the tonoplast was not affected by myosin XI-K inhibition. However, the normal tonoplast dynamics required myosin XI-K activity. These results reveal a new pathway of the myosin-dependent protein trafficking to PD that is hijacked by GFLV to promote tubule-guided transport of this virus between plant cells. To establish infection, plant viruses spread cell-to-cell via narrow channels in the cell wall, the plasmodesmata (PD). Movement proteins (MP) are virus-encoded proteins essential for virus intercellular transport through PD. Plasmodesmata located plant proteins (PDLPs), are specifically recognised by the MPs of tubule-forming viruses. Here we show that PDLP targeting to PD depends on the molecular motors myosin XI-K and XI-2. Consistently, and in support of a function of PDLP as PD receptor for MP, overexpression of dominant negative myosin mutants inhibits tubule formation by Grapevine fanleaf virus (GFLV) MP and dramatically reduces virus movement.
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影响因子：
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