Pilder S, Moore M, Logan J, Shenk T
Mol Cell Biol. 1986 Feb;6(2):470-6. doi: 10.1128/mcb.6.2.470-476.1986.
The adenovirus type 5 mutant H5dl338 lacks 524 base pairs within early region 1B. The mutation removed a portion of the region encoding the related E1B-55K and -17K polypeptides but did not disturb the E1B-21K coding region. The virus can be propagated in 293 cells which contain and express the adenovirus type 5 E1A and E1B regions, but it is defective for growth in HeLa cells, in which its final yield is reduced about 100-fold compared with the wild-type virus. The mutant also fails to transform rat cells at normal efficiency. The site of the dl338 defect was studied in HeLa cells. Early gene expression and DNA replication appeared normal. Late after infection, mRNAs coded by the major late transcription unit accumulated to reduced levels. At a time when transcription rates and steady-state nuclear RNA species were normal, the rate at which late mRNA accumulated in the cytoplasm was markedly reduced. Furthermore, in contrast to the case with the wild type, transport and accumulation of cellular mRNAs continued late after infection with dl338. Thus, the E1B product appears to facilitate transport and accumulation of viral mRNAs late after infection while blocking the same processes for cellular mRNAs.
5型腺病毒突变体H5dl338在早期区域1B内缺失524个碱基对。该突变去除了编码相关E1B-55K和-17K多肽的区域的一部分,但未干扰E1B-21K编码区。该病毒可在含有并表达5型腺病毒E1A和E1B区域的293细胞中增殖,但在HeLa细胞中生长存在缺陷,其最终产量与野生型病毒相比降低约100倍。该突变体也不能以正常效率转化大鼠细胞。在HeLa细胞中研究了dl338缺陷的位点。早期基因表达和DNA复制看起来正常。感染后期,主要晚期转录单位编码的mRNA积累水平降低。在转录速率和稳态核RNA种类正常的时候,晚期mRNA在细胞质中积累的速率明显降低。此外,与野生型情况相反,感染dl338后晚期细胞mRNA的转运和积累仍在继续。因此,E1B产物似乎在感染后期促进病毒mRNA的转运和积累,同时阻断细胞mRNA的相同过程。