Control of baculovirus polyhedrin gene expression by very late factor 1.
Control of baculovirus polyhedrin gene expression by very late factor 1.
复制标题
极晚因子 1 对杆状病毒多角体蛋白基因表达的控制。
DOI：
10.1006/viro.1998.9272
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发表时间：
1998
期刊：
影响因子：
3.7
通讯作者：
Miller,LK
中科院分区：
文献类型：
--
作者：
Yang,S;Miller,LK
vlf-1是一个杆状病毒基因，它调节非常晚的基因表达（J.R. McLachlin和L. K.米勒，J.病毒学，68，7746-7756，1994），并且在苜蓿银纹夜蛾核型多角体病毒（AcMNPV）（S. Yang和L. K.米勒，“杆状病毒极晚期因子1（vlf-1）基因的表达和突变分析。”Virology，245，99-109，1998）。为了研究VLF-1表达对杆状病毒感染的影响，我们构建了仅表达低水平VLF-1的重组病毒和在不同启动子控制下的VLF-1重组体。具有产生低水平VLF-1的VLF-1突变等位基因的病毒正常复制病毒的出芽形式，但不产生封闭体。因此，需要比支持出芽病毒生产所需的更高浓度的VLF-1来激活非常晚的基因表达。通过改变vlf-1表达的水平和/或时间，多角体蛋白基因（polh）表达的时间，通常发生在感染的很晚，可以提前或延迟。vlf-1的早期过表达增加了polh启动子的表达水平，但导致细胞过早解体。数据表明，VLF-1是极晚期基因表达的限制因素，并且VLF-1的水平控制着闭塞的发生。
vlf-1is a baculovirus gene that regulates very late gene expression (J. R. McLachlin and L. K. Miller,J. Virol.,68, 7746–7756, 1994) and also plays a crucial role in the replication of the budded form ofAutographa californicanuclear polyhedrosis virus (AcMNPV) (S. Yang and L. K. Miller, “Expression and mutational analysis of the baculovirus very late factor 1 (vlf-1) gene.”Virology,245, 99–109, 1998). To examine the influence ofvlf-1expression on baculovirus infection, we constructed recombinant viruses that expressed only low levels of VLF-1 and recombinants withvlf-1under the control of different promoters. Viruses with mutant alleles ofvlf-1that produced low levels of VLF-1 replicated the budded form of the virus normally but produced no occlusion bodies. Thus, a higher concentration of VLF-1 was needed to activate very late gene expression than was needed to support budded virus production. By altering the level and/or timing ofvlf-1expression, the timing of polyhedrin gene (polh) expression, which normally occurs very late in infection, could be advanced or delayed. Early overexpression ofvlf-1increased the level of expression from thepolhpromoter but caused premature cellular disintegration. The data indicate that VLF-1 is the limiting factor in very late gene expression and that the level of VLF-1 controls the onset of occlusion.