Steinhoff C, Schulz W A
Urologische Klinik und Biologisch-Medizinisches Forschungszentrum, Heinrich-Heine-Universität, 40225 Düsseldorf, Germany.
Mol Genet Genomics. 2003 Dec;270(5):394-402. doi: 10.1007/s00438-003-0931-2. Epub 2003 Oct 7.
Although LINE-1 (L1) sequences constitute the most important family of retrotransposons in the human genome, their transcriptional regulation is poorly understood. Specifically, their unusual internal promoter is incompletely characterized. Current promoter prediction programs fail to identify the promoter in the 5'UTR of the active LINE-1 element L1.2B. Experimental investigation of this promoter using reporter gene assays in various human and murine cell types confirmed that the promoter consists of two segments, and demonstrated that the distal portion is essential for cell-type-independent activity. No differences in promoter activity were found between normal and transformed cells. The complete promoter was shown to possess approximately 20% of the activity of the strong early promoter of cytomegalovirus, and to be capable of directing the expression of levels of p53 sufficient to kill normal and transformed human cells. Thus, active LINE-1 elements contain highly active promoters capable of driving cell-type-independent expression, which are of potential use in mammalian expression constructs. In vitro methylation of the promoter at HpaII sites decreased its activity independently of cell type, but this repression was alleviated in MBD2-/- cells. Surprisingly, mutation of specific HpaII sites was also found to reduce promoter activity. Thus, efficient repression of the L1.2B promoter by DNA methylation may involve MBD2 binding, but at least one HpaII site also appears to be involved specifically in transcriptional activation. Since neither promoter activity nor the efficiency of repression by methylation differed between normal and tumor cells, the re-activation of LINE-1 sequences observed in tumor cells is probably caused by hypomethylation of the promoter.
尽管LINE-1(L1)序列是人类基因组中最重要的逆转座子家族,但其转录调控仍知之甚少。具体而言,其异常的内部启动子特征尚不完整。当前的启动子预测程序无法识别活跃的LINE-1元件L1.2B的5'UTR中的启动子。在各种人类和小鼠细胞类型中使用报告基因检测对该启动子进行的实验研究证实,该启动子由两个片段组成,并表明远端部分对于细胞类型非依赖性活性至关重要。在正常细胞和转化细胞之间未发现启动子活性的差异。完整的启动子显示具有约20%的巨细胞病毒强早期启动子的活性,并且能够指导足以杀死正常和转化的人类细胞的p53水平的表达。因此,活跃的LINE-1元件包含能够驱动细胞类型非依赖性表达的高活性启动子,这在哺乳动物表达构建体中具有潜在用途。启动子在HpaII位点的体外甲基化独立于细胞类型降低了其活性,但在MBD2 -/-细胞中这种抑制作用得到缓解。令人惊讶的是,还发现特定HpaII位点的突变会降低启动子活性。因此,DNA甲基化对L1.2B启动子的有效抑制可能涉及MBD2结合,但至少一个HpaII位点似乎也特别参与转录激活。由于正常细胞和肿瘤细胞之间启动子活性以及甲基化抑制效率均无差异,肿瘤细胞中观察到的LINE-1序列的重新激活可能是由启动子的低甲基化引起的。