Cell-to-cell movement of Potato Potexvirus X is dependent on suppression of RNA silencing
Cell-to-cell movement of Potato Potexvirus X is dependent on suppression of RNA silencing
复制标题
DOI：
10.1111/j.1365-313x.2005.02539.x
复制
发表时间：
2005-11-01
期刊：
影响因子：
7.2
通讯作者：
Baulcombe, DC
中科院分区：
文献类型：
--
作者：
Bayne, EH;Rakitina, DV;Baulcombe, DC
在转基因和病毒感染的植物中，RNA沉默涉及一个可移动的沉默信号，该信号可以在细胞间和系统地通过植物移动。人们认为这种信号可以影响病毒的远距离运动，因为病毒基因组中编码的沉默蛋白抑制子是病毒远距离运动所必需的。然而，直到现在，人们还不知道移动信号是否也能影响细胞间的短程病毒运动。本文通过对马铃薯马铃薯痘病毒X （PVX）沉默抑制子P25的随机突变分析，我们提供了证据证明它确实如此。所有沉默抑制缺陷的突变体在病毒细胞间运动中也没有功能。然而，我们发现突变的P25蛋白作为沉默抑制因子而不是作为运动蛋白，我们得出结论，沉默抑制不足以允许病毒在细胞之间运动：必须有第二个P25功能独立于沉默，但也是细胞间运动所必需的。与这一假设相一致，我们发现了两类抑制因子失活的P25突变体。其中一类突变体被认为具有辅助功能，因为它们不能支持PVX的运动，可以由异源的沉默抑制子来补充。第二类P25突变体被认为具有抑制因子和第二功能缺陷，因为异源沉默抑制因子不能恢复病毒运动。基于对短干扰RNA积累的分析，P25可能通过干扰RNA沉默效应复合物的组装或功能来抑制沉默。
RNA silencing in transgenic and virus-infected plants involves a mobile silencing signal that can move cell-to-cell and systemically through the plant. It is thought that this signal can influence long-distance movement of viruses because protein suppressors of silencing encoded in viral genomes are required for long-distance virus movement. However, until now, it was not known whether the mobile signal could also influence short-range virus movement between cells. Here, through random mutation analysis of the Potato Potexvirus X (PVX) silencing suppressor P25, we provide evidence that it does. All mutants that were defective for silencing suppression were also non-functional in viral cell-to-cell movement. However, we identified mutant P25 proteins that were functional as silencing suppressors but not as movement proteins and we conclude that suppression of silencing is not sufficient to allow virus movement between cells: there must be a second P25 function that is independent of silencing but also required for cell-to-cell movement. Consistent with this hypothesis, we identified two classes of suppressor-inactive P25 mutants. One class of these mutants is proposed to be functional for the accessory function because their failure to support PVX movement could be complemented by heterologous suppressors of silencing. The second class of P25 mutants is considered defective for both the suppressor and second functions because the heterologous silencing suppressors did not restore virus movement. It is possible, based on analyses of short interfering RNA accumulation, that P25 suppresses silencing by interfering with either assembly or function of the effector complexes of RNA silencing.