Bingle C D, Gitlin J D
Edward Mallinckrodt Department of Pediatrics, Washington University School of Medicine, St. Louis, MO 63110.
Biochem J. 1993 Oct 1;295 ( Pt 1)(Pt 1):227-32. doi: 10.1042/bj2950227.
To determine the mechanisms of cell-specific gene expression in the developing pulmonary epithelium the Clara cell secretory protein (CCSP) gene promoter was analysed by DNAase I footprinting. A prominent site of protein-DNA interaction was detected from nucleotides -132 to -76 using nuclear extract from mouse lung and human H441 cells. Mobility shift analysis revealed that an oligonucleotide corresponding to this region interacted with multiple proteins from lung and H441 cell nuclear extracts. Analysis of the nucleotide sequence of this region identified two potential binding sites for hepatocyte nuclear factor 3 (HNF-3), and consistent with this finding binding to this CCSP oligonucleotide was specifically competed for by an oligonucleotide corresponding to the HNF-3-binding site from the mouse transthyretin gene. Mobility shift of the CCSP oligonucleotide was supershifted using antisera specific to HNF-3 alpha and HNF-3 beta, and HNF-3 alpha and HNF-3 beta translated in vitro were found to bind specifically to this same oligonucleotide. Co-transfection of HNF-3 alpha- and HNF-3 beta-expression plasmids increased cell-specific reporter gene activity in H441 cells transfected with a CCSP-CAT gene chimeric construct containing this -132 to -76 region. Taken together, these results suggest a role for HNF-3 in mediating cell-specific CCSP gene expression within the bronchiolar epithelium. These findings support the hypothesis that members of the HNF-3 'forkhead' family of transcription factors determine gene expression and cell fate in multiple cell lineages derived from the primitive gut endoderm.
为了确定发育中的肺上皮细胞特异性基因表达的机制,通过DNA酶I足迹法分析了克拉拉细胞分泌蛋白(CCSP)基因启动子。使用小鼠肺和人H441细胞核提取物,在核苷酸-132至-76处检测到一个显著的蛋白质-DNA相互作用位点。迁移率变动分析表明,与该区域对应的寡核苷酸与肺和H441细胞核提取物中的多种蛋白质相互作用。对该区域核苷酸序列的分析确定了两个潜在的肝细胞核因子3(HNF-3)结合位点,与此发现一致,与该CCSP寡核苷酸的结合被对应于小鼠甲状腺素运载蛋白基因中HNF-3结合位点的寡核苷酸特异性竞争。使用针对HNF-3α和HNF-3β的特异性抗血清使CCSP寡核苷酸的迁移率发生超迁移,并且发现体外翻译的HNF-3α和HNF-3β特异性结合该相同的寡核苷酸。用包含该-132至-76区域的CCSP-CAT基因嵌合构建体转染的H441细胞中,共转染HNF-3α和HNF-3β表达质粒可增加细胞特异性报告基因活性。综上所述,这些结果表明HNF-3在介导细支气管上皮细胞特异性CCSP基因表达中起作用。这些发现支持以下假设:转录因子HNF-3“叉头”家族的成员决定了源自原始肠内胚层的多个细胞谱系中的基因表达和细胞命运。