Thompson T, Fan H
Department of Molecular Biology and Biochemistry, University of California, Irvine 92717.
Virus Genes. 1988 Oct;2(1):83-98. doi: 10.1007/BF00569738.
The chromatin structure of chimeric Moloney murine leukemia viruses (M-MuLVs) containing a glucocorticoid response element (GRE) from mouse mammary tumor virus (MMTV) inserted into the long terminal repeat (LTR) was investigated. Nuclear run-on assays indicated that transcription from the chimeric proviruses was induced 2- to 4-fold by dexamethasone. The wild-type M-MuLV 5' LTR contained a DNase I hypersensitive (HS) site at the TATA sequences, as well as four sites in the enhancer region. The chimeric LTRs contained these sites, as well as three additional sites in the MMTV sequences. Two of the MMTV sites were present in the absence of hormone, while one was hormone-induced. In addition, internal MMTV sequences appeared protected from DNase I digestion in the absence of hormone, suggesting bound protein. Hormone treatment resulted in loss of the DNase I protection.
对嵌合型莫洛尼鼠白血病病毒（M-MuLV）的染色质结构进行了研究，该病毒的长末端重复序列（LTR）中插入了来自小鼠乳腺肿瘤病毒（MMTV）的糖皮质激素反应元件（GRE）。核转录分析表明，地塞米松可使嵌合前病毒的转录增加2至4倍。野生型M-MuLV 5' LTR在TATA序列处含有一个DNase I超敏（HS）位点，在增强子区域还有四个位点。嵌合LTR包含这些位点，以及MMTV序列中的另外三个位点。其中两个MMTV位点在无激素时就存在，而另一个是激素诱导产生的。此外，在无激素时，MMTV内部序列似乎受到保护，免受DNase I消化，提示有结合蛋白存在。激素处理导致DNase I保护作用丧失。
