Panning B, Smiley J R
Pathology Department, McMaster University, Hamilton, Ontario, Canada.
Mol Cell Biol. 1993 Jun;13(6):3231-44. doi: 10.1128/mcb.13.6.3231-3244.1993.
We found that transcription of endogenous human Alu elements by RNA polymerase III was strongly stimulated following infection of HeLa cells with adenovirus type 5, leading to the accumulation of high levels of Alu transcripts initiated from Alu polymerase III promoters. In contrast to previously reported cases of adenovirus-induced activation of polymerase III transcription, induction required the E1b 58-kDa protein and the products of E4 open reading frames 3 and 6 in addition to the 289-residue E1a protein. In addition, E1a function was not required at high multiplicities of infection, suggesting that E1a plays an indirect role in Alu activation. These results suggest previously unsuspected regulatory properties of the adenovirus E1b and E4 gene products and provide a novel approach to the study of the biology of the most abundant class of dispersed repetitive DNA in the human genome.
我们发现,在用5型腺病毒感染HeLa细胞后,RNA聚合酶III对内源人类Alu元件的转录受到强烈刺激,导致从Alu聚合酶III启动子起始的高水平Alu转录本积累。与先前报道的腺病毒诱导的聚合酶III转录激活情况不同,除了289个氨基酸的E1a蛋白外,诱导还需要E1b 58-kDa蛋白以及E4开放阅读框3和6的产物。此外,在高感染复数时不需要E1a功能,这表明E1a在Alu激活中起间接作用。这些结果提示了腺病毒E1b和E4基因产物以前未被怀疑的调控特性,并为研究人类基因组中最丰富的一类分散重复DNA的生物学特性提供了一种新方法。