Nakamura T, Nakajima T, Tsunoda S, Nakada S, Oda K, Tsurui H, Wada A
Department of Physics, Faculty of Science, University of Tokyo, Japan.
J Virol. 1992 Nov;66(11):6436-50. doi: 10.1128/JVI.66.11.6436-6450.1992.
The level of fibronectin (FN) gene expression is very high in resting rat 3Y1 cells but greatly decreased in adenovirus E1-transformed cells. To study the mechanism of this down-regulation, nuclear factors binding to the 5'-flanking region of the FN gene were analyzed by gel retardation assay and DNase I footprinting. Nuclear factors that were present in the transformed cells but nearly absent in resting 3Y1 cells interacted with multiple sites of the promoter region. Oligonucleotide competition with the FN promoter-chloramphenicol acetyltransferase (CAT) reporter constructs (pFCAT) for these factors in the transformed cells indicated that all of them had a negative effect on FN gene expression. Of them, a factor(s) (G10BP) binding to the G10 stretch from positions -239 to -230 and to two GC boxes consisting of the G10 stretch with one internal C residue insertion from positions -105 to -95 and -54 to -44 had the strongest repressive activity. Introduction of substitutive mutations into these G-rich sequences resulted in the increase in CAT activity of pFCAT in the transformed cells. The recognition sequences of G10BP and Sp1 overlap in two GC boxes. G10BP has stronger affinity for heparin and GC boxes than does Sp1, suggesting that G10BP may repress FN gene transcription by displacing Sp1.
纤连蛋白(FN)基因在静止的大鼠3Y1细胞中表达水平非常高,但在腺病毒E1转化的细胞中则大幅下降。为了研究这种下调的机制,通过凝胶阻滞试验和DNase I足迹法分析了与FN基因5'侧翼区域结合的核因子。在转化细胞中存在但在静止的3Y1细胞中几乎不存在的核因子与启动子区域的多个位点相互作用。用FN启动子-氯霉素乙酰转移酶(CAT)报告基因构建体(pFCAT)对这些因子在转化细胞中进行寡核苷酸竞争实验表明,它们对FN基因表达均有负面影响。其中,一种与从-239至-230位的G10序列以及由G10序列与一个内部C残基插入组成的两个GC盒结合的因子(G10BP),其结合位点分别为-105至-95位和-54至-44位,具有最强的抑制活性。在这些富含G的序列中引入替代突变导致转化细胞中pFCAT的CAT活性增加。G10BP和Sp1的识别序列在两个GC盒中重叠。G10BP对肝素和GC盒的亲和力比Sp1更强,这表明G10BP可能通过取代Sp1来抑制FN基因转录。