Oh C K, Neurath M, Cho J J, Semere T, Metcalfe D D
Department of Pediatrics, Harbor-UCLA Medical Center, Torrance, CA 90509, USA.
Biochem J. 1997 Apr 15;323 ( Pt 2)(Pt 2):511-9. doi: 10.1042/bj3230511.
T-cell activation gene 3 (TCA3) encodes a beta-chemokine that is transcriptionally regulated in mast cells; the gene has a functional NF-kappaB element at positions -194 to -185. The 5'-flanking region of this gene is also known to have a negative regulatory region between -2057 and -1342. To characterize the negative regulatory elements (NREs), this region was sequenced and then digested by HindIII enzyme into two fragments, NRE-1 (-2057 to -1493) and NRE-2 (-1492 to -1342). Both NRE-1 and NRE-2 in the 5'-3' orientation inhibited chloramphenicol acetyltransferase (CAT)-protein synthesis by a TCA3-CAT construct transfected into mast cells that were then activated. Only NRE-1 inhibited CAT-protein synthesis in the 3'-5' orientation. Further deletion of the 5' region of NRE-1 partially abolished the inhibitory activity. Both NRE-1 and NRE-2 inhibited the activity of a CD20-CAT construct independent of cell activation. Electrophoretic mobility shift assays showed DNA-protein complex formation with subsequences (CCCCCATTCT) of NRE-1 (NRE-1a) and (CCATGA) of NRE-2 (NRE-2b). NRE-1a appears to be novel. NRE-2b is identical with a putative silencer motif in the alphaIIb integrin gene. Site-directed mutagenesis demonstrated that both NRE-1a and NRE-2b are important in the negative regulation of TCA3 promoter activity. In vivo ligation-mediated PCR footprinting of the NRE-2 region revealed protection between -1372 and -1354, which contains NRE-2b. The data thus demonstrate identity of a silencer motif, here termed NRE-2b, in both the alphaIIb integrin gene and the TCA3, and that this silencer region in mast cells is functional both in vivo and in vitro. Further, evidence is presented that the promoter for TCA3 contains a novel silencer motif, termed NRE-1a, characterized by a CT-rich sequence.
T细胞激活基因3(TCA3)编码一种在肥大细胞中受转录调控的β趋化因子;该基因在-194至-185位有一个功能性的核因子κB元件。已知该基因的5'侧翼区在-2057至-1342之间有一个负调控区。为了鉴定负调控元件(NREs),对该区域进行测序,然后用HindIII酶消化成两个片段,即NRE-1(-2057至-1493)和NRE-2(-1492至-1342)。5'至3'方向的NRE-1和NRE-2均通过转染到随后被激活的肥大细胞中的TCA3-CAT构建体抑制氯霉素乙酰转移酶(CAT)蛋白的合成。只有NRE-1在3'至5'方向抑制CAT蛋白的合成。进一步缺失NRE-1的5'区域会部分消除其抑制活性。NRE-1和NRE-2均独立于细胞激活抑制CD20-CAT构建体的活性。电泳迁移率变动分析显示,NRE-1的亚序列(CCCCCATTCT)(NRE-1a)和NRE-2的(CCATGA)(NRE-2b)形成了DNA-蛋白质复合物。NRE-1a似乎是新发现的。NRE-2b与αIIb整合素基因中的一个假定沉默子基序相同。定点诱变表明,NRE-1a和NRE-2b在TCA3启动子活性的负调控中都很重要。对NRE-2区域进行体内连接介导的PCR足迹分析显示,在-1372至-1354之间存在保护作用,该区域包含NRE-2b。因此,数据证明了αIIb整合素基因和TCA3中一个沉默子基序(此处称为NRE-2b)的一致性,并且肥大细胞中的这个沉默子区域在体内和体外均具有功能。此外,有证据表明TCA3的启动子包含一个新的沉默子基序,称为NRE-1a,其特征是富含CT的序列。