Wang K L, Warner J R
Department of Cell Biology, Albert Einstein College of Medicine, The Bronx, New York 10461, USA.
Mol Cell Biol. 1998 Jul;18(7):4368-76. doi: 10.1128/MCB.18.7.4368.
Reb1p is a DNA binding protein of Saccharomyces cerevisiae that has been implicated in the activation of transcription by polymerase (Pol) II, in the termination of transcription by Pol I, and in the organization of nucleosomes. Studies of the transcriptional control of the REB1 gene have led us to identify three Reb1p binding sites in the 5' region of the its gene, termed A, B, and C, at positions -110, -80, and +30 with respect to transcription initiation. In vitro, Reb1p binds to the three sites with the relative affinity of A >/= C > B. Kinetic parameters suggest that when both A and C sites are present on the same DNA molecule, the C site may recruit Reb1p for the A site. In vivo the A and B sites each contribute to the transcription activity of REB1 in roughly additive fashion. Mutation of both A and B sites abolishes transcription. On the other hand, the C site is a negative element, reducing transcription by 40%. In cells overexpressing Reb1p, the C site reduces transcription by more than 80%. This effect can be transposed to another transcription unit, demonstrating that the effect of Reb1p binding at the C site does not depend on interaction with upstream Reb1p molecules. Relocation of the C site to a position 105 bp downstream of the transcription initiation site abolishes its effect, suggesting that it does not act as a conventional attenuator of transcription. We conclude that binding of Reb1p at the C site hinders formation of the initiation complex. This arrangement of Reb1p binding sites provides a positive and negative mechanism to autoregulate the expression of REB1. Such an arrangement could serve to dampen the inevitable fluctuation in Rep1p levels caused by the intermittent presence of its mRNA within an individual cell.
Reb1p是酿酒酵母中的一种DNA结合蛋白,它与聚合酶(Pol)II转录的激活、Pol I转录的终止以及核小体的组织有关。对REB1基因转录调控的研究使我们在其基因的5'区域鉴定出三个Reb1p结合位点,分别称为A、B和C,相对于转录起始位点位于-110、-80和+30位置。在体外,Reb1p以A≥C>B的相对亲和力结合这三个位点。动力学参数表明,当A和C位点同时存在于同一DNA分子上时,C位点可能会为A位点招募Reb1p。在体内,A和B位点各自以大致累加的方式对REB1的转录活性有贡献。A和B位点的突变会消除转录。另一方面,C位点是一个负调控元件,使转录减少40%。在过表达Reb1p的细胞中,C位点使转录减少超过80%。这种效应可以转移到另一个转录单元,表明Reb1p在C位点的结合效应不依赖于与上游Reb1p分子的相互作用。将C位点重新定位到转录起始位点下游105 bp处会消除其效应,这表明它不是作为传统的转录衰减子起作用。我们得出结论,Reb1p在C位点的结合会阻碍起始复合物的形成。Reb1p结合位点的这种排列提供了一种正负机制来自动调节REB1的表达。这样的排列可以用来抑制由单个细胞内其mRNA间歇性存在导致的Reb1p水平不可避免波动。