Currie R A
Laboratory of Gene Regulation, Picower Institute for Medical Research, Manhasset, New York 11030, USA.
J Biol Chem. 1998 Jan 16;273(3):1430-4. doi: 10.1074/jbc.273.3.1430.
The ubiquitous transcription factor, NF-Y, plays a pivotal role in the cell cycle regulation of the mammalian cyclin A, cdc25C, and cdc2 genes, in the S-phase activation of the ribonucleotide reductase R2 gene, in addition to its critical role as a key proximal promoter factor in the transcriptional regulation of the albumin, collagen, lipoprotein lipase, major histocompatibility complex class II, and a variety of other eukaryotic and viral genes. In this report, the NF-Y complex has been shown to possess histone acetyltransferase activity through physical association with the related histone acetyltransferase enzymes, human GCN5 and P/CAF in vivo. The assembled NF-YA:B:C complex, and the NF-YB:YC, NF-YB:YC (DNA binding-subunit interaction domain), and NF-YC:YB (DNA binding-subunit interaction domain) heterodimers were sufficient to support stable interaction with human GCN5 in vitro, suggesting that these histone acetyltransferases interact with a unique surface in the ancient YB:YC histone-fold motif. Deletion of either N- or C-terminal regions in human GCN5 disrupted interaction with NF-Y in vitro. In addition, human GCN5 was observed to activate NF-Y in transient transfections in vivo using a natural alpha 2(I) collagen promoter. These results suggest that these associated histone acetyltransferases may serve to modulate NF-Y transactivation potential by aiding disruption of local chromatin structure thereby facilitating NF-Y access to its CCAAT box DNA binding sites.
普遍存在的转录因子NF-Y在哺乳动物细胞周期蛋白A、细胞周期蛋白依赖性激酶25C(cdc25C)和细胞周期蛋白依赖性激酶2(cdc2)基因的细胞周期调控中起关键作用,在核糖核苷酸还原酶R2基因的S期激活中也起关键作用,此外,它还是白蛋白、胶原蛋白、脂蛋白脂肪酶、主要组织相容性复合体II类以及多种其他真核和病毒基因转录调控中的关键近端启动子因子。在本报告中,已证明NF-Y复合物在体内通过与相关组蛋白乙酰转移酶人GCN5和P/CAF的物理结合而具有组蛋白乙酰转移酶活性。组装好的NF-YA:B:C复合物以及NF-YB:YC、NF-YB:YC(DNA结合亚基相互作用域)和NF-YC:YB(DNA结合亚基相互作用域)异二聚体在体外足以支持与人类GCN5的稳定相互作用,这表明这些组蛋白乙酰转移酶与古老的YB:YC组蛋白折叠基序中的独特表面相互作用。人GCN5中N端或C端区域的缺失在体外破坏了与NF-Y的相互作用。此外,在体内使用天然α2(I)胶原蛋白启动子进行瞬时转染时,观察到人类GCN5可激活NF-Y。这些结果表明,这些相关的组蛋白乙酰转移酶可能通过帮助破坏局部染色质结构来调节NF-Y的反式激活潜能,从而促进NF-Y与其CCAAT框DNA结合位点的结合。