White R J, Stott D, Rigby P W
Laboratory of Eukaryotic Molecular Genetics, National Institute for Medical Research, Mill Hill, London, UK.
EMBO J. 1990 Nov;9(11):3713-21. doi: 10.1002/j.1460-2075.1990.tb07584.x.
Transcription by RNA polymerase III of the B2 family of middle-repetitive elements is activated in response to transformation by a variety of agents, including DNA tumour viruses, RNA tumour viruses and chemical carcinogens. We have investigated the mechanism of activation in SV40-transformed cells and we find that the effect is due to an increase in the activity of the general class III transcription factor TFIIIC, achieved both by an increase in factor abundance and by a change in its phosphorylation state. SV40 transformation also stimulates transcription of other genes by RNA polymerase III but the effect may be balanced by compensatory post-transcriptional changes. TFIIIC may mediate the stimulation of polymerase III transcription by a range of transforming viruses.
在受到多种致癌因素(包括DNA肿瘤病毒、RNA肿瘤病毒和化学致癌物)转化后,中重复序列B2家族会被RNA聚合酶III转录激活。我们研究了SV40转化细胞中的激活机制,发现这种效应是由于通用III类转录因子TFIIIC的活性增加,这是通过因子丰度的增加及其磷酸化状态的改变实现的。SV40转化还会刺激RNA聚合酶III对其他基因的转录,但这种效应可能会被转录后补偿性变化所平衡。TFIIIC可能介导一系列转化病毒对聚合酶III转录的刺激作用。