Fujita N, Takebayashi S, Okumura K, Kudo S, Chiba T, Saya H, Nakao M
Department of Tumor Genetics and Biology, Kumamoto University School of Medicine, Kumamoto 860-0811, Japan.
Mol Cell Biol. 1999 Sep;19(9):6415-26. doi: 10.1128/MCB.19.9.6415.
DNA methylation of promoter-associated CpG islands is involved in the transcriptional repression of vertebrate genes. To investigate the mechanisms underlying gene inactivation by DNA methylation, we characterized a human MBD1 protein, one of the components of MeCP1, which possesses a methyl-CpG binding domain (MBD) and cysteine-rich (CXXC) domains. Four novel MBD1 isoforms (MBD1v1, MBD1v2, MBD1v3, and MBD1v4) were identified by the reverse transcription-PCR method. We found that these transcripts were alternatively spliced in the region of CXXC domains and the C terminus. Green fluorescent protein-fused MBD1 was localized to multiple foci on the human genome, mostly in the euchromatin regions, and particularly concentrated in the pericentromeric region of chromosome 1. Both the MBD sequence and genome methylation were required for proper localization of the MBD1 protein. We further investigated whether MBD1 isoforms are responsible for transcriptional repression of human genes. A bacterially expressed MBD1 protein bound preferentially to methylated DNA fragments containing CpG islands from the tumor suppressor genes p16, VHL, and E-cadherin and from an imprinted SNRPN gene. All MBD1 isoforms inhibited promoter activities of these genes via methylation. Interestingly, MBD1 isoforms v1 and v2 containing three CXXC domains also suppressed unmethylated promoter activities in mammalian cells. These effects were further manifested in Drosophila melanogaster cells, which lack genome methylation. Sp1-activated transcription of methylated p16 and SNRPN promoters was inhibited by all of the MBD1 isoforms, whereas the isoforms v1 and v2 reduced Sp1-activated transcription from unmethylated promoters as well. These findings suggested that the MBD1 isoforms have different roles in methylation-mediated transcriptional silencing in euchromatin.
启动子相关CpG岛的DNA甲基化参与脊椎动物基因的转录抑制。为了研究DNA甲基化导致基因失活的机制,我们对人MBD1蛋白进行了表征,它是MeCP1的组成成分之一,具有甲基化CpG结合结构域(MBD)和富含半胱氨酸的结构域(CXXC)。通过逆转录PCR方法鉴定出四种新的MBD1异构体(MBD1v1、MBD1v2、MBD1v3和MBD1v4)。我们发现这些转录本在CXXC结构域和C末端区域发生选择性剪接。绿色荧光蛋白融合的MBD1定位于人类基因组上的多个位点,主要位于常染色质区域,尤其集中在1号染色体的着丝粒周围区域。MBD1蛋白的正确定位需要MBD序列和基因组甲基化。我们进一步研究了MBD1异构体是否负责人类基因的转录抑制。细菌表达的MBD1蛋白优先结合来自肿瘤抑制基因p16、VHL和E-钙黏蛋白以及印记基因SNRPN的含有CpG岛的甲基化DNA片段。所有MBD1异构体均通过甲基化抑制这些基因的启动子活性。有趣的是,含有三个CXXC结构域的MBD1异构体v1和v2也抑制哺乳动物细胞中未甲基化的启动子活性。这些效应在缺乏基因组甲基化的果蝇细胞中进一步体现。所有MBD1异构体均抑制Sp1激活的甲基化p16和SNRPN启动子的转录,而v1和v2异构体也降低了Sp1激活的未甲基化启动子的转录。这些发现表明,MBD1异构体在常染色质中甲基化介导的转录沉默中具有不同作用。