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在保护胚胎干细胞身份方面,H3K9甲基化编写器及其阅读器HP1之间的功能交叉声响

Lixia Dong¹, Huaqi Liao¹, Linchun Zhao¹

¹State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center, Medical School of Nanjing University, Nanjing, China.

Stem cell reports

|September 13, 2023

概括

失去HP1蛋白减少了H3K9甲基化写作者,导致胚胎干细胞 (ESC) 失去多能性. 恢复Setdb1,Nanog和Oct4拯救了ESC的身份,揭示了关键的作家-读者合作.

科学领域:

表观遗传学和基因调节
干细胞生物学干细胞生物学
染色体的动态染色体的动态

背景情况:

基因组H3氨酸9 (H3K9) 甲基化是一种关键的表观遗传标记,它定义了异色素蛋白,并影响了细胞命运.
HP1蛋白是H3K9甲基化读者,但它们与H3K9甲基化写者的精确相互作用仍然不完全理解.
胚胎干细胞 (ESC) 依赖精确的表观遗传控制来维持多能性和调节血统承诺.

研究的目的:

阐明H3K9甲基化编写者和读者之间的功能相互作用,以保持ESC身份.
研究H3K9甲基化阅读器 (HP1家族) 损失对ESC多能性和基因表达的后果.
确定ESC身份和表观遗传状态调节的反循环中涉及的关键因素.

主要方法:

产生和描述HP1缺陷的ESC (Hp1-零ESC).
对H3K9甲基化水平的定量分析和关键多能性因子的表达 (例如,Setdb1,Nanog,Oct4).
涉及突变ESC中特定基因异位表达的救援实验.
评估ESC身份和血统特定的基因表达变化.

主要成果:

失去HP1蛋白质导致H3K9甲基转移酶的表达减少,特别是Setdb1.1.
Hp1-null ESCs 退出多能性,表现出降低的 Nanog 和 Oct4 表达,并获得血统特定的特征.
Setdb1,Nanog和Oct4的异胎表达可以挽救Hp1-null ESCs的多能性和身份.
Setdb1 除复制ESC身份的丧失,同时减少HP1 基因表达,突出一个相互调节循环.

结论:

在H3K9甲基化写入器 (例如,Setdb1) 和读取器 (HP1蛋白) 之间存在一个合作的反循环,以保护ESC身份.
HP1蛋白对于维持H3K9甲基化机制的表达至关重要,这反过来又保持了多能性.
破坏这种作家-读者合作会导致社会经济委员会差异化和自我更新能力的丧失.

关键词:

在G9A中,G9A是G9A 这是GLP,GLP就是GLP.在H3K9甲基化过程中.在HP1中,HP1是HP1.在SETDB1中,我们可以使用SETDB1.交叉语音交叉语音交叉语音交叉语音交叉语音胚胎干细胞是一种胚胎干细胞.胚胎层的谱系胚胎层的谱系多能性的多能性.更多关于裁员裁员

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