Kohwi Y, Kohwi-Shigematsu T
La Jolla Cancer Research Foundation, California 92037.
Genes Dev. 1991 Dec;5(12B):2547-54. doi: 10.1101/gad.5.12b.2547.
We examined the participation of triplex DNA structure in gene regulation using a poly(dG)-poly(dC) sequence as a model. We show that a poly(dG)-poly(dC) sequence, which can adopt an intramolecular dG.dG.dC triplex under superhelical strain, strongly augments gene expression when placed 5' to a promoter. The activity of this sequence exhibits a striking length dependency: dG tracts of 27-30 bp augment the expression of a reporter gene to a level comparable to that observed with the polyoma enhancer in mouse LTK- cells, whereas tracts of 35 bp and longer have virtually no effect. A supercoiled plasmid containing a dG tract of 30 bp competes in vivo for a trans-acting factor as revealed by reduction in the reporter gene transcription driven by the (dG)29/promoter of the test plasmid, while dGs of 35 bp and longer in the competition plasmid failed to compete. In purified supercoiled plasmid DNA at a superhelical density of -0.05, dG tracts of 32 bp and longer form a triplex, whereas those of 30 bp and shorter remain double-stranded under a PBS solution. These results suggest that a localized superhelical strain can exist, at least transiently, in mouse LTK- cells, and before being relaxed by topoisomerases this rapidly induces dG tracts of 35 bp and longer to adopt a triplex preventing the factor from binding. Thus, these data suggest that a poly(dG)-poly(dC) sequence can function as a negative regulator by adopting an intramolecular triple helix structure in vivo.
我们以聚(dG)-聚(dC)序列为模型,研究了三链体DNA结构在基因调控中的作用。我们发现,聚(dG)-聚(dC)序列在超螺旋张力下可形成分子内dG·dG·dC三链体,当置于启动子的5'端时,能强烈增强基因表达。该序列的活性呈现出显著的长度依赖性:27 - 30 bp的dG片段可将报告基因的表达增强至与小鼠LTK - 细胞中多瘤病毒增强子相当的水平,而35 bp及更长的片段几乎没有作用。含有30 bp dG片段的超螺旋质粒在体内可与一种反式作用因子竞争,这可通过测试质粒的(dG)29/启动子驱动的报告基因转录减少得以揭示,而竞争质粒中35 bp及更长的dG片段则无法竞争。在超螺旋密度为 -0.05的纯化超螺旋质粒DNA中,32 bp及更长的dG片段形成三链体,而30 bp及更短的片段在PBS溶液中仍保持双链状态。这些结果表明,在小鼠LTK - 细胞中可能至少短暂存在局部超螺旋张力,在被拓扑异构酶松弛之前,这种张力会迅速诱导35 bp及更长的dG片段形成三链体,从而阻止因子结合。因此,这些数据表明聚(dG)-聚(dC)序列在体内可通过形成分子内三螺旋结构发挥负调控作用。