THE PRODUCT OF GENE US11 OF HERPES-SIMPLEX VIRUS TYPE-1 IS EXPRESSED AS A TRUE LATE GENE
THE PRODUCT OF GENE US11 OF HERPES-SIMPLEX VIRUS TYPE-1 IS EXPRESSED AS A TRUE LATE GENE
复制标题
DOI：
10.1099/0022-1317-67-5-871
复制
发表时间：
1986-05-01
影响因子：
3.8
通讯作者：
EVERETT, RD
中科院分区：
文献类型：
--
作者：
JOHNSON, PA;MACLEAN, C;EVERETT, RD
1 型单纯疱疹病毒 (HSV-1) 的基因可分为至少三个时间调控组，称为立即早期 (IE)、早期和晚期。我们详细研究了晚期基因类别成员 US11 的表达，该基因编码表观分子量 21K 的多肽。在存在和不存在膦酰乙酸（一种病毒 DNA 复制抑制剂）的情况下，使用高度特异性和灵敏的探针来监测组织培养细胞的 HSV-1 感染期间的 US11 RNA 和蛋白质合成。结果与编码糖蛋白 D (gD) 的延迟早期基因 US6 的产物的类似研究进行了比较。结果发现US11的RNA和蛋白质合成模式与gD显着不同。 US11产物出现较晚，并积累至感染后期，而gD RNA在后期显着减少。在 DNA 合成抑制剂存在的情况下，US11 基因表达降低了 50 至 100 倍，而 gD 表达降低了 5 至 10 倍。我们得出结论，US11 在 HSV-1 感染期间表现为真正的晚期基因。然而，敏感检测的使用允许在旨在消除 DNA 复制的条件下检测极低水平的 US11 基因产物，这引发了人们对 DNA 复制对于表达真正的晚期 HSV-1 基因的绝对要求的质疑。这些结果根据晚期基因表达调控的当前模型进行了讨论。
The genes of herpes simplex virus type 1 (HSV-1) can be divided into at least three temporally regulated groups termed immediate early (IE), early and late. We have studied in detail the expression of a member of the late class of genes, US11, which encodes a polypeptide of apparent molecular weight 21K. Highly specific and sensitive probes were used to monitor US11 RNA and protein synthesis during HSV-1 infection of tissue culture cells in the presence and absence of phosphonoacetic acid, an inhibitor of viral DNA replication. The results were compared with a similar study of the products of a delayed early gene, US6, encoding glycoprotein D (gD). It was found that the patterns of RNA and protein synthesis from US11 were significantly different to those of gD. US11 products appeared later and accumulated until late in infection, while gD RNA was significantly reduced at late times. In the presence of the inhibitor of DNA synthesis, US11 gene expression was reduced 50- to 100-fold while gD expression was reduced five- to tenfold. We concluded that US11 behaves as a true late gene during HSV-1 infection. However, the use of sensitive assays, which allowed the detection of very low levels of US11 gene products under conditions designed to eliminate DNA replication, brings into question the absolute requirement for DNA replication for the expression of a true late HSV-1 gene. These results are discussed in terms of current models for the regulation of late gene expression.