AN ADENOVIRUS EARLY REGION-4 GENE-PRODUCT IS REQUIRED FOR INDUCTION OF THE INFECTION-SPECIFIC FORM OF CELLULAR E2F ACTIVITY
AN ADENOVIRUS EARLY REGION-4 GENE-PRODUCT IS REQUIRED FOR INDUCTION OF THE INFECTION-SPECIFIC FORM OF CELLULAR E2F ACTIVITY
复制标题
DOI：
10.1101/gad.3.7.1062
复制
发表时间：
1989-07-01
影响因子：
10.5
通讯作者：
SHENK, T
中科院分区：
文献类型：
--
作者：
HARDY, S;ENGEL, DA;SHENK, T
E2F是一种细胞内的、序列特异性的DNA结合因子，它与出现在E1a和E2早期mRNA帽位点上游的一对位点结合。在腺病毒感染期间，有一种形式的E2F被诱导，它协同结合到E2控制区的一对位点上。感染特异性E2F活性的产生依赖于早期区域4(E4)，因为感染了缺乏E4的突变体的细胞提取液不包含这种活性。相反，在E4突变体中发现了两种新的E2F形式。感染突变病毒后一段时间不能使E1a基因产生野生型感染特异的E2F活性。E1B-55kD-、E1B-21kD-、E2-72kD-和E3-编码区突变对感染特异性E2F的产生无影响。对细胞系的分析证实了突变病毒的结果。表达E1a但不表达E4基因的细胞(例如293细胞)不含有感染特异性E2F。表达E4基因的细胞系含有这种活性。这些观察结果表明，E4参与了感染诱导的E2F结合活性的变化。这些数据与E1a在这一过程中发挥的间接作用一致，它通过介导E4基因产物的有效表达，进而诱导E2F活性的改变。
E2f is a cellular, sequence-specific DNA-binding factor that binds to pairs of sites that occur upstream of the E1A and E2 early mRNA cap sites. During adenovirus infection, there is induction of a form of E2F that binds cooperatively to the pair of sites in the E2 control region. Production of the infection-specific E2F activity is dependent on early region 4(E4), as extracts of cells infected with a mutant that lacks E4 did not contain this activity. Instead, two new forms of E2F were seen with the E4 mutant. Infection with mutant viruses unable to make E1A gene produced the wild-type infection-specific E2F activity after a delay. Mutations in the E1B-55 kD-, E1B-21 kD-, E2-72 kD-, and E3-coding regions had no effect on production of infection-specific E2F. Analysis of cell line confirmed the results obtained with mutant virsus. Cells that expressed E1A but not E4 genes (e.g., 293 cells) did not contain infection-specific E2F. Cell lines that expressed the E4 gene contained the activity. These observations demonstrate that E4 participates in the infection-induced change in E2F-binding activity. The data consistent with E1A playing an indirect role in the process by mediating the efficient expression of E4 gene products which, in turn, induce the alteration in E2F activity.