Disch D L, Rader T A, Cresci S, Leone T C, Barger P M, Vega R, Wood P A, Kelly D P
Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Mol Cell Biol. 1996 Aug;16(8):4043-51. doi: 10.1128/MCB.16.8.4043.
Expression of the gene encoding medium-chain acyl coenzyme A dehydrogenase (MCAD), a nuclearly encoded mitochondrial fatty acid beta-oxidation enzyme, is regulated in parallel with fatty acid oxidation rates among tissues and during development. We have shown previously that the human MCAD gene promoter contains a pleiotropic element (nuclear receptor response element [NRRE-1]) that confers transcriptional activation or repression by members of the nuclear receptor superfamily. Mice transgenic for human MCAD gene promoter fragments fused to a chloramphenicol acetyltransferase gene reporter were produced and characterized to evaluate the role of NRRE-1 and other promoter elements in the transcriptional control of the MCAD gene in vivo. Expression of the full-length MCAD promoter-chloramphenicol acetyltransferase transgene (MCADCAT.371) paralleled the known tissue-specific differences in mitochondrial beta-oxidation rates and MCAD expression. MCADCAT.371 transcripts were abundant in heart tissue and brown adipose tissue, tissues with high-level MCAD expression. During perinatal cardiac developmental stages, expression of the MCADCAT.371 transgene paralleled mouse MCAD mRNA levels. In contrast, expression of a mutant MCADCAT transgene, which lacked NRRE-1 (MCADCATdeltaNRRE-1), was not enriched in heart or brown adipose tissue and did not exhibit appropriate postnatal induction in the developing heart. Transient-transfection studies with MCAD promoter-luciferase constructs containing normal or mutant NRRE-1 sequences demonstrated that the nuclear receptor binding sequences within NRRE-1 are necessary for high-level transcriptional activity in primary rat cardiocytes. Electrophoretic mobility shift assays demonstrated that NRRE-1 was bound by several cardiac and brown adipose nuclear proteins and that these interactions required the NRRE-1 receptor binding hexamer sequences. Antibody supershift studies identified the orphan nuclear receptor COUP-TF as one of the endogenous cardiac proteins which bound NRRE-1. These results dictate an important role for nuclear receptors in the transcriptional control of a nuclear gene encoding a mitochondrial fatty acid oxidation enzyme and identify a gene regulatory pathway involved in cardiac energy metabolism.
中链酰基辅酶A脱氢酶(MCAD)是一种核编码的线粒体脂肪酸β-氧化酶,其编码基因的表达在不同组织间以及发育过程中与脂肪酸氧化速率呈平行调节。我们之前已经表明,人类MCAD基因启动子包含一个多效元件(核受体反应元件[NRRE-1]),该元件可介导核受体超家族成员的转录激活或抑制作用。我们构建了与人MCAD基因启动子片段融合的氯霉素乙酰转移酶基因报告基因的转基因小鼠,并对其进行了表征,以评估NRRE-1和其他启动子元件在体内MCAD基因转录调控中的作用。全长MCAD启动子-氯霉素乙酰转移酶转基因(MCADCAT.371)的表达与线粒体β-氧化速率和MCAD表达中已知的组织特异性差异平行。MCADCAT.371转录本在心脏组织和棕色脂肪组织中丰富,这两种组织中MCAD表达水平较高。在围产期心脏发育阶段,MCADCAT.371转基因的表达与小鼠MCAD mRNA水平平行。相比之下,缺乏NRRE-1的突变型MCADCAT转基因(MCADCATdeltaNRRE-1)的表达在心脏或棕色脂肪组织中未富集,并且在发育中的心脏中未表现出适当的出生后诱导。用含有正常或突变NRRE-1序列的MCAD启动子-荧光素酶构建体进行的瞬时转染研究表明,NRRE-1内的核受体结合序列对于原代大鼠心肌细胞中的高水平转录活性是必需的。电泳迁移率变动分析表明,NRRE-1与几种心脏和棕色脂肪核蛋白结合,并且这些相互作用需要NRRE-1受体结合六聚体序列。抗体超迁移研究确定孤儿核受体COUP-TF是与NRRE-1结合的内源性心脏蛋白之一。这些结果表明核受体在编码线粒体脂肪酸氧化酶的核基因的转录调控中起重要作用,并确定了一条参与心脏能量代谢的基因调控途径。