Wu F, Lee A S
Department of Biochemistry and Molecular Biology, Keck School of Medicine, University of Southern California, Los Angeles, California 90089-9176, USA.
J Biol Chem. 2001 Jan 5;276(1):28-34. doi: 10.1074/jbc.M006074200.
In analyzing cis-regulatory elements important for cell cycle control of the replication-dependent hamster histone H3.2 gene, we discovered a binding site for the transcription factor YY1 embedded within GC-rich sequences between the two tandem CCAAT repeats proximal to the TATA element. Base mutations that specifically eliminated YY1 binding resulted in suppression of the S phase induction of the H3.2 promoter. In addition, we discovered that YY1 is an interactive partner of AP-2, which also binds the H3.2 promoter and regulates its cell cycle-dependent expression. The critical domains for YY1 and AP-2A interaction are mapped, revealing that the N-terminal portion of YY1 (amino acids 1-300) and the DNA-binding/dimerization region of AP-2A are required. Our results suggest that YY1, acting as a transcription factor binding to its site on the promoter, or through protein-protein interaction with AP-2, may be part of a regulatory network including key cell cycle regulators such as c-Myc and Rb in controlling growth- and differentiation-regulated gene expression.
在分析对依赖复制的仓鼠组蛋白H3.2基因的细胞周期控制至关重要的顺式调控元件时,我们在靠近TATA元件的两个串联CCAAT重复序列之间富含GC的序列中发现了转录因子YY1的一个结合位点。特异性消除YY1结合的碱基突变导致H3.2启动子的S期诱导受到抑制。此外,我们发现YY1是AP-2的一个相互作用伙伴,AP-2也结合H3.2启动子并调节其细胞周期依赖性表达。绘制了YY1与AP-2A相互作用的关键结构域,发现需要YY1的N端部分(氨基酸1-300)和AP-2A的DNA结合/二聚化区域。我们的结果表明,YY1作为一种转录因子与其在启动子上的位点结合,或通过与AP-2的蛋白质-蛋白质相互作用,可能是包括c-Myc和Rb等关键细胞周期调节因子在内的调控网络的一部分,参与控制生长和分化调节的基因表达。