Jones R M, Branda J, Johnston K A, Polymenis M, Gadd M, Rustgi A, Callanan L, Schmidt E V
Massachusetts General Hospital Cancer Center, Charlestown, 02129, USA.
Mol Cell Biol. 1996 Sep;16(9):4754-64. doi: 10.1128/MCB.16.9.4754.
The mRNA cap-binding protein (eukaryotic initiation factor 4E [eIF4E]) binds the m7 GpppN cap on mRNA, thereby initiating translation. eIF4E is essential and rate limiting for protein synthesis. Overexpression of eIF4E transforms cells, and mutations in eIF4E arrest cells in G, in cdc33 mutants. In this work, we identified the promoter region of the gene encoding eIF4E, because we previously identified eIF4E as a potential myc-regulated gene. In support of our previous data, a minimal, functional, 403-nucleotide promoter region of eIF4E was found to contain CACGTG E box repeats, and this core eIF4E promoter was myc responsive in cotransfections with c-myc. A direct role for myc in activating the eIF4E promoter was demonstrated by cotransfections with two dominant negative mutants of c-myc (MycdeltaTAD and MycdeltaBR) which equally suppressed promoter function. Furthermore, electrophoretic mobility shift assays demonstrated quantitative binding to the E box motifs that correlated with myc levels in the electrophoretic mobility shift assay extracts; supershift assays demonstrated max and USF binding to the same motif. cis mutations in the core or flank of the eIF4E E box simultaneously altered myc-max and USF binding and inactivated the promoter. Indeed, mutations of this E box inactivated the promoter in all cells tested, suggesting it is essential for expression of eIF4E. Furthermore, the GGCCACGTG(A/T)C(C/G) sequence is shared with other in vivo targets for c-myc, but unlike other targets, it is located in the immediate promoter region. Its critical function in the eIF4E promoter coupled with the known functional significance of eIF4E in growth regulation makes it a particularly interesting target for c-myc regulation.
mRNA帽结合蛋白(真核生物起始因子4E [eIF4E])与mRNA上的m7GpppN帽结合,从而启动翻译过程。eIF4E对于蛋白质合成至关重要且是限速因素。eIF4E的过表达会使细胞发生转化,而在cdc33突变体中,eIF4E的突变会使细胞停滞在G期。在本研究中,我们确定了编码eIF4E的基因的启动子区域,因为我们之前将eIF4E鉴定为一个潜在的受myc调控的基因。为支持我们之前的数据,发现eIF4E的一个最小的、功能性的403个核苷酸的启动子区域包含CACGTG E盒重复序列,并且这个核心eIF4E启动子在与c-myc共转染时对myc有反应。与c-myc的两个显性负性突变体(MycdeltaTAD和MycdeltaBR)共转染证明了myc在激活eIF4E启动子中起直接作用,这两个突变体同样抑制了启动子功能。此外,电泳迁移率变动分析表明与E盒基序的定量结合与电泳迁移率变动分析提取物中的myc水平相关;超迁移分析表明max和USF与相同基序结合。eIF4E E盒核心或侧翼的顺式突变同时改变了myc-max和USF的结合并使启动子失活。事实上,该E盒的突变在所有测试细胞中均使启动子失活,表明它对于eIF4E的表达至关重要。此外,GGCCACGTG(A/T)C(C/G)序列与c-myc的其他体内靶点共有,但与其他靶点不同的是,它位于紧邻的启动子区域。其在eIF4E启动子中的关键功能以及eIF4E在生长调控中的已知功能意义使其成为c-myc调控的一个特别有趣的靶点。