Argentin S, Ardati A, Tremblay S, Lihrmann I, Robitaille L, Drouin J, Nemer M
Institut de recherches cliniques de Montréal, Université de Montréal, Québec, Canada.
Mol Cell Biol. 1994 Jan;14(1):777-90. doi: 10.1128/mcb.14.1.777-790.1994.
Cardiac myocytes undergo a major genetic switch within the first week of postnatal development, when cell division ceases terminally and many cardiac genes are either activated or silenced. We have developed stage-specific cardiocyte cultures to analyze transcriptional control of the rat atrial natriuretic factor (ANF) gene to identify the mechanisms underlying tissue-specific and developmental regulation of this gene in the heart. The first 700 bp of ANF flanking sequences was sufficient for cardiac muscle- and stage-specific expression in both atrial and ventricular myocytes, and a cardiac muscle-specific enhancer was localized between -136 and -700 bp. Deletion of this enhancer markedly reduced promoter activity in cardiac myocytes and derepressed ANF promoter activity in nonexpressing cells. Two distinct domains of the enhancer appeared to contribute differentially to cardiac specificity depending on the differentiation stage of the myocytes. DNase I footprinting of the enhancer domain active in differentiated cells revealed four putative regulatory elements including an A+T-rich region and a CArG element. Deletion mutagenesis and promoter reconstitution assays revealed an important role for the CArG-containing element exclusively in cardiac cells, where its activity was switched on in differentiated myocytes. Transcriptional activity of the ANF-CArG box correlated with the presence of a cardiac- and stage-specific DNA-binding complex which was not recognized by the c-fos serum response element. Thus, the use of this in vitro model system representing stage-specific cardiac development unraveled the presence of different regulatory mechanisms for transcription of the ANF gene during cardiac differentiation and may be useful for studying the regulatory pathways of other genes that undergo switching during cardiac myogenesis.
心肌细胞在出生后发育的第一周内经历重大的基因转换,此时细胞分裂最终停止,许多心脏基因被激活或沉默。我们开发了阶段特异性心肌细胞培养物,以分析大鼠心房利钠因子(ANF)基因的转录调控,从而确定该基因在心脏中组织特异性和发育调控的潜在机制。ANF侧翼序列的前700 bp足以在心房和心室肌细胞中实现心肌特异性和阶段特异性表达,并且一个心肌特异性增强子定位于-136至-700 bp之间。删除该增强子会显著降低心肌细胞中的启动子活性,并使非表达细胞中的ANF启动子活性去抑制。根据心肌细胞的分化阶段,增强子的两个不同结构域似乎对心脏特异性有不同的贡献。对分化细胞中活跃的增强子结构域进行DNA酶I足迹分析,揭示了四个推定的调控元件,包括一个富含A+T的区域和一个CArG元件。缺失诱变和启动子重组分析揭示了含CArG元件仅在心脏细胞中起重要作用,其活性在分化的心肌细胞中被开启。ANF-CArG盒的转录活性与一种心脏和阶段特异性DNA结合复合物的存在相关,该复合物不被c-fos血清反应元件识别。因此,使用这个代表阶段特异性心脏发育的体外模型系统,揭示了心脏分化过程中ANF基因转录存在不同的调控机制,并且可能有助于研究其他在心肌发生过程中经历转换的基因的调控途径。