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在体细胞核转移后的胚胎发育受到持续的基因素甲基化阻碍

Shogo Matoba¹, Yuting Liu¹, Falong Lu¹

¹Howard Hughes Medical Institute, Harvard Medical School, WAB-149G, 200 Longwood Avenue, Boston, MA 02115, USA; Program in Cellular and Molecular Medicine, Boston Children's Hospital, Harvard Medical School, WAB-149G, 200 Longwood Avenue, Boston, MA 02115, USA; Department of Genetics, Harvard Medical School, WAB-149G, 200 Longwood Avenue, Boston, MA 02115, USA.

|November 24, 2014

概括

基因组H3氨酸9三甲基化 (H3K9me3) 阻碍体细胞核转移 (SCNT) 克隆效率. 在捐赠细胞中去除H3K9me3显著提高了SCNT重编程和胚胎发育,提供了一个新的克隆策略.

科学领域:

表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
发育生物学发展生物学
生殖科学生殖科学

背景情况:

哺乳动物卵细胞具有将体细胞重新编程成全能状态的能力,这一过程对于通过体细胞核转移 (SCNT) 进行动物克隆至关重要.
在SCNT的一个重大障碍是克隆胚胎的高失败率,这归因于对重新编程缺陷的理解不足.
基质子修饰,特别是H3K9me3,越来越多地被认为是细胞重编程和发育潜力的关键调节者.

研究的目的:

识别特定的表观遗传因素,这些因素是SCNT有效重编程的障碍.
研究素H3氨酸9三甲基化 (H3K9me3) 在SCNT介导的重编程缺陷中的作用.
开发战略,克服表观遗传障碍,提高哺乳动物克隆的效率.

主要方法:

对SCNT和体外受精 (IVF) 胚胎进行比较转录组分析,以确定重编程耐药区域 (RRR).
评估 H3K9me3 在捐赠体细胞的RRR中的丰富.
利用捐赠细胞中H3K9me3脱甲基酶 (Kdm4d) 的异位表达和H3K9甲基转移酶的枯竭来评估它们对SCNT效率的影响.

主要成果:

已识别的RRRs通常在试管婴儿胚胎中表达,但在SCNT胚胎中沉默,在供体体细胞中为H3K9me3进行丰富.
宫外表达Kdm4d成功地去除了H3K9me3,重新激活了RRR,并显著提高了SCNT的效率.
缺乏H3K9甲基转移酶的捐赠体内核也导致了SCNT效率的显著提高.

结论:

基因组H3氨酸9三甲基化 (H3K9me3) 是一个关键的表观遗传障碍,阻碍了SCNT过程中高效的重编程.
在捐赠细胞中准和去除H3K9me3代表了一种有前途的治疗策略,以提高哺乳动物克隆效率.
这项研究为全能性表观遗传调节提供了新的见解,并为改进SCNT技术提供了潜在的突破.

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