small RNA mediated DNA methylation

小RNA介导的DNA甲基化

• 批准号: 24770167
• 负责人: IPPEI Nagamori
• 金额: $ 2.91万
• 依托单位: Osaka University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2012
• 资助国家: 日本
• 起止时间: 2012-04-01 至 2014-03-31
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-24770167/
• 关键词: DNAメチル化; PIWI; MILI; MIWI2; piRNA; レトロトランスポゾン; 核膜

Retrotransposon occupies approximately 40% of genome DNA, and it is widely known that DNA methylation mediated retrotransposon repressions are critical for mammal. During male germ cell differentiation, DNA methylation is globally erased, followed by obtaining DNA methylation at site specific manner, including Retrotransposon. Since DNA methylation causes gene repression, site specificity of DNA methylation is critical, however, it remains elusive how site specificity of DNA methylation is determined. By genetic analysis, Mili and Miwi2 were identified as important genes for to determine site specificity for DNA methylation, however, the precise molecular mechanisms are largely unknown. In this project, I have reported how MILI and MIWI2 contribute to site specificity of DNA methylation for retrotransposon

逆转录座子占基因组DNA的约40％，众所周知，DNA甲基化介导的逆转录子抑制作用对于哺乳动物至关重要。在男性生殖细胞分化过程中，DNA甲基化被全局擦除，然后以特定方式（包括逆转录座子）获得DNA甲基化。由于DNA甲基化会导致基因抑制，因此DNA甲基化的位点特异性至关重要，但是，如何确定DNA甲基化的位点特异性仍然难以捉摸。通过遗传分析，MILI和MIWI2被确定为确定DNA甲基化位点特异性的重要基因，但是，精确的分子机制在很大程度上是未知的。在这个项目中，我报道了Mili和Miwi2如何促进DNA甲基化的位点特异性