Chung K C, Huang D, Chen Y, Short S, Short M L, Zhang Z, Jungmann R A
Department of Cellular and Molecular Biology, Northwestern University Medical School, Chicago, Illinois 60611, USA.
Mol Cell Biol. 1995 Nov;15(11):6139-49. doi: 10.1128/MCB.15.11.6139.
The cyclic AMP (cAMP)-inducible promoter from the rat lactate dehydrogenase A subunit gene (LDH A) is associated with a distal negative regulatory element (LDH-NRE) that represses inherent basal and cAMP-inducible promoter activity. The element is of dyad symmetry, consisting of a palindromic sequence with two half-sites, 5'-TCTTG-3'. It represses the expression of an LDH A/chloramphenicol acetyltransferase (CAT) reporter gene in a dose-dependent, orientation- and position-independent fashion, suggesting that it is a true silencer element. Uniquely, it selectively represses cAMP-responsive element (CRE)-dependent transcription but has no effect on promoters lacking a CRE sequence. The repressing action of LDH-NRE could be overcome by cotransfection with LDH A/CAT vector oligonucleotides containing either the LDH-NRE or CRE sequence. This suggests that the reversal of repression was caused by the removal of functional active, limiting transacting factors which associate with LDH-NRE as well as with CRE. Gel mobility shift, footprinting, and Southwestern blotting assays demonstrated the presence of a 69-kDa protein with specific binding activity for LDH-NRE. Additionally, gel supershift assays with anti-CREB and anti-Fos antibodies indicate the presence of CREB and Fos or antigenically closely related proteins with the LDH-NRE/protein complex. We suggest that the LDH-NRE and CRE modules functionally interact to achieve negative modulation of cAMP-responsive LDH A transcriptional activity.
大鼠乳酸脱氢酶A亚基基因(LDH A)的环磷酸腺苷(cAMP)诱导型启动子与一个远端负调控元件(LDH-NRE)相关联,该元件可抑制固有的基础启动子活性和cAMP诱导型启动子活性。该元件具有二元对称性,由一个回文序列组成,包含两个半位点,即5'-TCTTG-3'。它以剂量依赖性、方向和位置无关的方式抑制LDH A/氯霉素乙酰转移酶(CAT)报告基因的表达,表明它是一个真正的沉默子元件。独特的是,它选择性地抑制cAMP反应元件(CRE)依赖性转录,但对缺乏CRE序列的启动子没有影响。通过与含有LDH-NRE或CRE序列的LDH A/CAT载体寡核苷酸共转染,可以克服LDH-NRE的抑制作用。这表明抑制作用的逆转是由于去除了与LDH-NRE以及CRE相关的功能性活性限制反式作用因子。凝胶迁移率变动分析、足迹分析和蛋白质印迹分析表明存在一种对LDH-NRE具有特异性结合活性的69 kDa蛋白。此外,用抗CREB和抗Fos抗体进行的凝胶超迁移分析表明,在LDH-NRE/蛋白复合物中存在CREB和Fos或抗原性密切相关的蛋白。我们认为,LDH-NRE和CRE模块在功能上相互作用,以实现对cAMP反应性LDH A转录活性的负调控。