Tobacco mosaic virus infection spreads cell to cell as intact replication complexes
Tobacco mosaic virus infection spreads cell to cell as intact replication complexes
复制标题
DOI：
10.1073/pnas.0401221101
复制
发表时间：
2004-04-20
影响因子：
11.1
通讯作者：
Beachy, RN
中科院分区：
文献类型：
--
作者：
Kawakami, S;Watanabe, Y;Beachy, RN
植物病毒编码运动蛋白（MP），通过胞间连丝促进感染的细胞-细胞转运。利用共聚焦显微镜观察了烟草花叶病毒（Tobacco mosaic virus，MV）侵染后12 ~ 36 h的完整叶片组织中病毒复制复合物（virusreplicationcomplex，VRC）在细胞内和细胞间的传播。从12 hpi开始，原代感染细胞中的VRC与皮质内质网相连，在14 hpi，表现出高的细胞内移动性（约160 nm/sec）;在14和16 hpi之间移动性减慢（约40 nm/sec），到18 hpi，VRC静止不动，邻近胞间连丝。VRC在18 - 20 hpi之间穿过胞间连丝。VRC的形成和移动过程在3-4 h内在相邻细胞中重复，而从原代感染细胞开始为20 h。血管内皮细胞的快速细胞内运动和扩散到邻近细胞被丝状肌动蛋白和肌球蛋白的抑制剂阻断，但不是由微管的抑制剂。我们提出了一个模型，即细胞间传播的TMV病毒感染是由亚病毒复制复合物，启动TMV复制后立即进入相邻的细胞。
Plant viruses encode movement proteins (MPs) that facilitate cell-cell transport of infection through plasmodesmata. Intracellular and intercellular spread of virus replication complexes (VRCs) of tobacco mosaic virus was followed in intact leaf tissue from 12 to 36 h post infection (hpi) by using confocal microscopy. From 12 hpi, VRCs in primary infected cells were associated with cortical endoplasmic reticulum, and at 14 hpi, exhibited high intracellular mobility (approximate to160 nm/sec); mobility was slowed between 14 and 16 hpi (approximate to40 nm/sec), and by 18 hpi, VRCs were stationary, adjacent to plasmodesmata. VRCs traversed the plasmodesmata between 18 and 20 hpi. The process of formation and movement of VRCs was repeated in adjacent cells in 3-4 h vs. 20 h from primary infected cells. The rapid intracellular movement of the VRCs and the spread to adjacent cells was blocked by inhibitors of filamentous actin and myosin, but not by inhibitors of microtubules. We propose a model whereby cell-cell spread of tobamovirus infection is accomplished by subviral replication complexes that initiate TMV replication immediately after entry to adjacent cells.