Pathway of assembly of herpesvirus capsids: an analysis using DNA+ temperature-sensitive mutants of pseudorabies virus.
Pathway of assembly of herpesvirus capsids: an analysis using DNA+ temperature-sensitive mutants of pseudorabies virus.
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疱疹病毒衣壳的组装途径：使用伪狂犬病病毒 DNA 温度敏感突变体进行分析。
DOI：
10.1016/0042-6822(82)90147-7
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发表时间：
1982
期刊：
影响因子：
3.7
通讯作者：
Ben-Porat,T
中科院分区：
文献类型：
--
作者：
Ladin,BF;Ihara,S;Hampl,H;Ben-Porat,T
据报道，九种不同的DNA+1 s突变体的Pr病毒都有缺陷的过程中，导致切割的多联体病毒DNA和核衣壳的形成。发现这些突变体中的六个在非允许温度下组装衣壳;三个是衣壳-（Ladinet等人，1980年）。在目前的通信中，我们进一步描述了这些突变体。每个突变体都被野生型病毒DNA的一个特异性限制性片段拯救，这表明这些突变体中没有一个在一个以上的基因座中发生改变。许多突变体以一定的频率相互补充，表明它们可能是在不同的基因中突变的。在非允许温度（41°）下用DNA+突变体感染的细胞合成了由野生型感染的细胞合成的所有病毒蛋白（如通过PAGE检测的），但有两个显著的例外：（1）ts 1感染的细胞合成了热不稳定的142 K衣壳蛋白。(2)在Ints 1、ts 109和tsJ（所有衣壳突变体）感染的细胞中，未积累可检测量的35 K衣壳蛋白。35 K衣壳蛋白通常由前体蛋白加工而成，加工后的蛋白仅在感染细胞的细胞核中可检测到。在被衣壳感染的细胞中，没有发生35 K蛋白前体的加工。此外，在所有衣壳感染的细胞中，所有衣壳蛋白在细胞核中的积累都受到损害。由于三种衣壳突变体中至少有两种在不同的基因中发生突变，我们得出结论，35 K蛋白的加工、衣壳组装和衣壳蛋白在核中的积累是相互依赖的事件，只有当衣壳组装所需的所有蛋白质都有功能时才会发生。在这些结果的基础上，我们提出，35 K蛋白在衣壳组装过程中被加工，并且将蛋白组装成衣壳是衣壳蛋白继续移动到感染细胞的细胞核中并在其中积累所必需的。
It was reported previously that nine different DNA+is mutants of Pr virus were all defective in the processes leading to the cleavage of concatemeric viral DNA and to the formation of nucleocapsids. Six of these mutants were found to assemble capsids at the nonpermissive temperature; three were capsid−(Ladinet al., 1980). In the present communication we have characterized these mutants further. Each of the mutants was rescued by one specific restriction fragment of wild type virus DNA indicating that none of these mutants is altered in more than one locus. Many of the mutants complemented one another well at a frequency indicating that they are probably mutated in different genes. Cells infected at the nonpermissive temperature (41°) with the DNA+mutants synthesized all the virus proteins synthesized by wild type-infected cells (as detected by PAGE) with two notable exceptions: (1)ts1-infected cells synthesized a thermolabile 142K capsid protein. (2) Ints1,ts109, andtsJ (all capsid−mutants)-infected cells, detectable amounts of 35K capsid protein did not accumulate. The 35 K capsid protein is normally processed from a precursor protein, the processed protein being detectable in the nucleus of the infected cells only. In capsid−-infected cells processing of the 35K protein precursor did not occur. Furthermore, accumulation in the nucleus of all capsid proteins was impaired in all the capsid−-infected cells. Because at least two of the three capsid−mutants are mutated in different genes, we conclude that the processing of the 35K protein, capsid assembly, and accumulation of capsid proteins in the nuclei are interdependent events which occur only if all the proteins necessary for capsid assembly are functional. On the basis of these results, we propose that the 35K protein is processed during capsid assembly and that assembly of the proteins into capsids is required for the continued movement of capsid proteins to, and their accumulation in, the nuclei of infected cells.
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影响因子：
5.4
作者：
B. Ladin;M. Blankenship;T. Ben‐Porat
通讯作者：
T. Ben‐Porat
疱疹病毒感染细胞中蛋白质的合成，VI。
DOI：
--
发表时间：
1970
影响因子：
11.1
作者：
A. Kaplan;T. Ben‐Porat
通讯作者：
T. Ben‐Porat
影响因子：
15.3
作者：
C. Morgan;S. A. Ellison;H. M. Rose;D. Moore
通讯作者：
D. Moore
影响因子：
5.4
作者：
JACOB, RJ;MORSE, LS;ROIZMAN, B
通讯作者：
ROIZMAN, B
影响因子：
3.7
作者：
BENPORAT, T;RIXON, FJ
通讯作者：
RIXON, FJ