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G10BP是Sp1的一种E1A诱导型负调节因子,可抑制大鼠纤连蛋白基因的转录。

G10BP, an E1A-inducible negative regulator of Sp1, represses transcription of the rat fibronectin gene.

作者信息

Suzuki M, Kuroda C, Oda E, Tsunoda S, Nakamura T, Nakajima T, Oda K

机构信息

Department of Biological Science and Technology, Science University of Tokyo, Noda, Japan.

出版信息

Mol Cell Biol. 1995 Oct;15(10):5423-33. doi: 10.1128/MCB.15.10.5423.

Abstract

Downregulation of the fibronectin (FN) gene in a rat 3Y1 derivative cell line, XhoC, transformed by the adenovirus E1A and E1B genes seems to be caused by the induction of a negative regulator, G10BP, which binds to three G-rich sequences in the promoter (T. Nakamura, T. Nakajima, S. Tsunoda, S. Nakada, K. Oda, H. Tsurui, and A. Wada, J. Virol. 66:6436-6450, 1992). These are the G10 stretch and two GC boxes consisting of the G10 stretch with one internal C residue insertion. The recognition sequences of G10BP and Sp1 (GGGCGG) overlap in these GC boxes. To analyze the mechanism of the downregulation, G10BP was purified by DNA affinity chromatography, and its molecular mass was estimated to be about 30 kDa. The promoter was modified by substituting the sequence GGGG with ATCC or CTTA in these G-rich sequences, leaving the Sp1 motif intact, and by replacing the Sp1 motif by the T stretch. Transcription of FN promoter-chloramphenicol acetyltransferase fusion genes carrying the base substitution in one or more of these G-rich sequences both in vivo and in vitro revealed that the base substitution in any G-rich sequence results in reduction of promoter activity, although the downstream GC box (GCd) plays a primary role. The addition of G10BP severely inhibited the activities of the FN promoters carrying the wild-type GCd in vitro, while the promoters carrying the mutant GCd were unaffected. The binding affinity of G10BP and Sp1 to each of the G-rich sequences, analyzed by gel shift assays, indicated that G10BP binds strongly to the GCd, moderately to the G10 stretch, and weakly to GCu, while Sp1 binds strongly to GCu, moderately to GCd, and weakly to the G10 stretch. Sp1 binding to GCd and the G10 stretch was inhibited by G10BP, while binding to GCu was unaffected. These results indicate that FN gene transcription is inhibited in XhoC cells primarily by exclusion of Sp1 binding to GCd by G10BP and that G10BP is a new class of Sp1 negative regulator.

摘要

在由腺病毒E1A和E1B基因转化的大鼠3Y1衍生细胞系XhoC中,纤连蛋白(FN)基因的下调似乎是由一种负调节因子G10BP的诱导引起的,该因子与启动子中的三个富含G的序列结合(T. Nakamura、T. Nakajima、S. Tsunoda、S. Nakada、K. Oda、H. Tsurui和A. Wada,《病毒学杂志》66:6436 - 6450,1992年)。这些序列是G10序列以及两个由G10序列插入一个内部C残基组成的GC盒。G10BP和Sp1(GGGCGG)的识别序列在这些GC盒中重叠。为了分析下调机制,通过DNA亲和层析纯化了G10BP,其分子量估计约为30 kDa。通过将这些富含G的序列中的GGGG替换为ATCC或CTTA来修饰启动子,同时保持Sp1基序完整,以及通过将Sp1基序替换为T序列。携带这些富含G的序列中一个或多个发生碱基替换的FN启动子 - 氯霉素乙酰转移酶融合基因在体内和体外的转录表明,任何富含G的序列中的碱基替换都会导致启动子活性降低,尽管下游GC盒(GCd)起主要作用。添加G10BP在体外严重抑制携带野生型GCd的FN启动子的活性,而携带突变型GCd的启动子不受影响。通过凝胶迁移实验分析G10BP和Sp1与每个富含G的序列的结合亲和力表明,G10BP与GCd强烈结合,与G10序列中度结合,与GCu弱结合,而Sp1与GCu强烈结合,与GCd中度结合,与G10序列弱结合。G10BP抑制Sp1与GCd和G10序列的结合,而与GCu的结合不受影响。这些结果表明,在XhoC细胞中FN基因转录主要是通过G10BP排除Sp1与GCd的结合来抑制的,并且G10BP是一类新的Sp1负调节因子。

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