Oskouian B, Rangan V S, Smith S
Children's Hospital Oakland Research Institute, 747 52nd Street, Oakland, CA 94609, USA.
Biochem J. 1997 May 15;324 ( Pt 1)(Pt 1):113-21. doi: 10.1042/bj3240113.
Sequence elements have been identified within the 1.2 kb-long first intron of the fatty acid synthase (FAS) gene that mediate both positive and negative effects on transcription. The negative regulatory element, when positioned downstream of either the FAS or simian virus 40 promoter, down-regulates the expression of a coupled reporter gene in an orientation-dependent manner. Sequences mediating this effect have been mapped, by deletion mutagenesis, to two regions approximately within nucleotides +405 to +768 and +924 to +1083. Both regions contain sequence elements that are strongly protected from DNase I digestion by nuclear extracts prepared from liver, but not by those prepared from spleen. The results of run-on assays performed with nuclei derived from tissues that express FAS at either high or low levels indicate that the different rates of transcription of the endogenous FAS gene result from differences in the extent of initiation, so it is unlikely that the negative effect is caused by transcriptional pausing in the first intron. The positive element maps to nt +292 to +297 and corresponds to an authentic binding site for upstream stimulatory factor (USF). This USF-binding element can up-regulate transcription from a heterologous promoter in a position- and orientation-independent manner. However, in the context of the entire FAS first intron, the effect of the USF-binding site is masked unless the effect of the negative elements is ablated by mutagenesis. These results suggest that the dominant negative element of the first intron may play a role in determining the tissue-specific expression of the FAS gene.
在脂肪酸合酶(FAS)基因1.2 kb长的首个内含子中已鉴定出一些序列元件,它们对转录具有正向和负向作用。当负调控元件位于FAS或猿猴病毒40启动子下游时,会以方向依赖的方式下调偶联报告基因的表达。通过缺失诱变已将介导这种效应的序列定位到两个区域,大约在核苷酸+405至+768以及+924至+1083范围内。这两个区域都包含一些序列元件,从肝脏制备的核提取物能强烈保护这些元件免受DNase I消化,而从脾脏制备的核提取物则不能。对来自高表达或低表达FAS的组织的细胞核进行的连续分析结果表明,内源性FAS基因不同的转录速率是由起始程度的差异导致的,因此负效应不太可能是由首个内含子中的转录暂停引起的。正向元件定位到核苷酸+292至+297,对应于上游刺激因子(USF)的一个真实结合位点。这个USF结合元件可以以位置和方向独立的方式上调来自异源启动子的转录。然而,在整个FAS首个内含子的背景下,除非通过诱变消除负元件的作用,否则USF结合位点的效应会被掩盖。这些结果表明,首个内含子的显性负元件可能在决定FAS基因的组织特异性表达中起作用。