Zinn K, Maniatis T
Cell. 1986 May 23;45(4):611-8. doi: 10.1016/0092-8674(86)90293-x.
We have used a DNAase I genomic footprinting procedure to detect interactions between cellular factors and the regulatory sequences of the human beta-interferon gene. Prior to induction with poly(I)-poly(C), factors that bind to DNA are detected in one region located between -94 and -167 from the mRNA cap site, and in another region located between -68 and -38. After induction these factors dissociate and another factor binds to a region located between -77 and -64. Correlation of these footprints with the effects of deletions in the regulatory region of the beta-interferon gene (accompanying paper) suggest that the factors that bind prior to induction are repressor molecules, while the component that binds after induction is a transcription factor. Dissociation of the repressor molecules from the DNA after induction may allow the transcription factor to bind to and activate the beta-interferon promoter. Thus, the beta-interferon gene may be controlled by a negative regulatory mechanism.
我们运用了DNA酶I基因组足迹法来检测细胞因子与人类β-干扰素基因调控序列之间的相互作用。在用聚肌苷酸-聚胞苷酸(poly(I)-poly(C))诱导之前,在距mRNA帽位点-94至-167之间的一个区域以及-68至-38之间的另一个区域检测到了与DNA结合的因子。诱导后,这些因子解离,另一个因子结合到-77至-64之间的区域。这些足迹与β-干扰素基因调控区域缺失效应(随附论文)的相关性表明,诱导前结合的因子是阻遏分子,而诱导后结合的成分是转录因子。诱导后阻遏分子从DNA上解离可能使转录因子能够结合并激活β-干扰素启动子。因此,β-干扰素基因可能受负调控机制控制。