Han M, Grunstein M
Molecular Biology Institute, University of California, Los Angeles 90024.
Cell. 1988 Dec 23;55(6):1137-45. doi: 10.1016/0092-8674(88)90258-9.
Nucleosome depletion can be made to occur in yeast by addition of glucose to strains containing the histone H4 gene under GAL promoter control. This leads to the activation of downstream promoter elements (TATA box and initiation, I, region) of three different regulated yeast promoters fused to the E. coli lacZ gene. Nucleosome loss activates the PHO5 downstream element in the presence or absence of the upstream activator sequences (UAS) through which PHO5 induction is normally mediated. The cytochrome C (CYC1) and galactokinase (GAL1) promoters are normally repressed by glucose through their UAS elements. However, when these UAS are deleted, the remaining downstream promoters are also activated by glucose-mediated nucleosome loss. These data suggest that nucleosome loss increases transcription initiation and subsequent elongation in vivo. They also indicate that the proteins which recognize the downstream promoter are activated and functional, at least in part, even in the absence of the UAS complex.
通过向含有在GAL启动子控制下的组蛋白H4基因的酵母菌株中添加葡萄糖，可使核小体缺失发生。这导致与大肠杆菌lacZ基因融合的三种不同调控的酵母启动子的下游启动子元件（TATA盒和起始I区）被激活。无论是否存在通常介导PHO5诱导的上游激活序列（UAS），核小体丢失都会激活PHO5下游元件。细胞色素C（CYC1）和半乳糖激酶（GAL1）启动子通常通过其UAS元件被葡萄糖抑制。然而，当这些UAS被缺失时，剩余的下游启动子也会被葡萄糖介导的核小体丢失激活。这些数据表明，核小体丢失增加了体内转录起始和随后的延伸。它们还表明，识别下游启动子的蛋白质即使在没有UAS复合物的情况下也至少部分被激活并具有功能。
