Tomilin N V, Iguchi-Ariga S M, Ariga H
Institute of Cytology, Academy of Sciences, Leningrad, USSR.
FEBS Lett. 1990 Apr 9;263(1):69-72. doi: 10.1016/0014-5793(90)80707-p.
Human cells contain a nuclear protein interacting with Alu repeats, and this protein seems to recognize a conserved sequence motif, GGAGGC, present within the RNA polymerase III promoter and within the SV40 T-antigen-dependent ARS-like element. To study the potential functional role of this element, we have inserted the sequence into a chloramphenicolacetyltransferase (CAT) expression vector with a SV40 promoter and enhancer element from the up-stream region of the human c-myc gene, and transfected HeLa cells with the resulting plasmid. Analysis of expression by the CAT assay indicates that the Alu-derived sequence supresses transcription of the CAT gene driven by the c-myc enhancer/SV40 promoter. The Alu-derived sequence also inhibits ARS activity of the c-myc enhancer. The data allow the explanation of the transcriptional inactivity of Alu repeats in HeLa cells, and suggest the existence of a negative control of Alu transcription.
人类细胞含有一种与Alu重复序列相互作用的核蛋白,这种蛋白似乎能识别一个保守的序列基序GGAGGC,该基序存在于RNA聚合酶III启动子内以及SV40 T抗原依赖性ARS样元件内。为了研究该元件的潜在功能作用,我们已将该序列插入到一个带有来自人类c-myc基因上游区域的SV40启动子和增强子元件的氯霉素乙酰转移酶(CAT)表达载体中,并用所得质粒转染HeLa细胞。通过CAT检测对表达进行分析表明,源自Alu的序列抑制了由c-myc增强子/SV40启动子驱动的CAT基因的转录。源自Alu的序列也抑制了c-myc增强子的ARS活性。这些数据有助于解释HeLa细胞中Alu重复序列的转录无活性,并提示存在对Alu转录的负调控。