REGULATION OF SV40 LATE TRANSCRIPTION BY LARGE T-ANTIGEN

猴病毒40（SV 40）晚期启动子可以被反式激活， 在没有DNA复制的情况下通过SV 40 T抗原。 转染实验表明，T抗原反式激活 可能涉及直接的启动子结合或诱导一种或 更多的细胞转录因子 与博士合作。 Peter Tegtmeyer我们已经证明了T抗原 结合位点I，以及II，在T-抗原结合依赖性 通路 为了进一步了解反式- 作用因子相互作用识别转录调节因子， 序列，我们已经检查了SV 40 T抗原和 腺病毒E1 A蛋白刺激腺病毒E2启动子。 化学合成的E2启动子突变体的功能是 一种诱导增强剂 通过插入5、10、15或20个碱基对， E2增强子中反向重复序列之间的非特异性DNA， 我们已经发现，一个特定的空间排列的序列上， E2启动子是反式激活所必需。

The simian virus 40 (SV40) late promoter can be trans-activated by SV40 T-antigen in the absence of DNA replication. Transfection experiments suggest that T-antigen trans-activation may involve either direct promoter binding or induction of one or more cellular transcription factors. In collaboration with Dr. Peter Tegtmeyer, we have demonstrated a role for T-antigen binding site I, as well as II, in the T-antigen binding dependent pathway. To gain further understanding of the mechanisms by which trans- acting factors interact to recognize transcriptional regulatory sequences, we have examined the ability of SV40 T-antigen and adenovirus E1A protein to stimulate the adenovirus E2 promoter. Chemically synthesized mutants of the E2 promoter function as an inducible enhancer. by insertion of 5, 10, 15 or 20 base pairs of non-specific DNA between inverted repeats in the E2 enhancer, we have found that a specific spatial arrangement of sequences on the E2 promoter are required for trans-activation.