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抑制DNA甲基转移酶 (Dnmt) 会导致存活胚胎中的Cdx2和Nanog水平增加

Fatma Uysal¹, Gozde Sukur², Nazlican Bozdemir¹

¹Ankara Medipol University School of Medicine, Department of Histology and Embryology, Ankara, Turkey.

The International journal of developmental biology

|June 5, 2023

概括

DNA甲基转移酶 (Dnmts) 对于胚胎发育至关重要. 在小鼠胚胎中击败Dnmt1或Dnmt3a破坏了细胞分化和存活,增加了自,ROS和亡的标志物.

科学领域:

表观遗传学和发育生物学
分子胚胎学分子胚胎学

背景情况:

表观遗传机制,特别是DNA甲基化,在不改变DNA序列的情况下调节基因表达.
DNA甲基转移酶 (Dnmts) 控制DNA甲基化模式,对细胞分化,生存和胚胎发育至关重要.
在植入前的发育过程中,Dnmt水平是动态调节的,影响细胞内细胞质 (ICM) 和体 (TE) 之间的细胞命运决定.

研究的目的:

研究Dnmt1和Dnmt3a在小鼠植入前胚胎发育中的作用.
分析Dnmt1和Dnmt3a淘汰对ICM/TE分化,自,活性氧物种 (ROS) 生产和亡的影响.

主要方法:

在小鼠囊中对Dnmt1和Dnmt3a的抑制.
胚胎培养时间为96小时.
测量Nanog (ICM标记物) 和Cdx2 (TE标记物) 的表达.
评估p62水平 (自标志物),ROS产量和亡 (TUNEL试验).

主要成果:

敲除Dnmt1或Dnmt3a显著增加了Nanog和Cdx2.2的表达.
沉默Dnmt1或Dnmt3a导致p62表达,ROS水平和亡的显著增加.
在植入前的发育过程中,DNAmt基因对于维持胚胎命运决定和细胞存活至关重要.

结论:

在早期小鼠胚胎中,Dnmt1和Dnmt3a在调节细胞分化和生存方面发挥着至关重要的作用.
破坏Dnmt功能会影响关键的细胞过程,包括自,ROS稳态和亡.
需要进一步的研究,以阐明胚胎发育中的Dnmt介导甲基化下游的具体目标.

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