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在具有跨基因CTCF边界删除的小鼠中发现了Igf2成年肌肉增强剂活性

Joanne L Thorvaldsen¹, Aimee M Juan¹, Yemin Lan¹

¹University of Pennsylvania Perelman School of Medicine, Epigenetics Institute, Department of Cell and Developmental Biology, Philadelphia, Pennsylvania, United States of America.

|August 29, 2025

概括

在新生儿肌肉中抑制Igf2基因. 它的去除在成年肌肉中双性激活Igf2,揭示了新的基因调节层.

科学领域:

遗传学和表观遗传学
基因调控
染色体生物学

背景情况:

印记基因表达依赖于印记控制区域 (ICR) 和增强剂-促进剂 (E-P) 相互作用.
该Igf2/H19位点使用ICR的CTCF结合来直接将增强剂接入到特定的促进体.
在Igf2调节中,CTCF结合的中央保存域 (CCD) 和相邻的lncRNA的作用尚未完全理解.

研究的目的:

调查CTCF结合的中心保存域 (CCD) 和Igf2/H19位点的相邻lncRNA的功能.
阐明CCD在调节Igf2表达中的作用,特别是在肌肉组织中.
了解CCD删除对Igf2基因激活和染色体结构的影响.

主要方法:

产生和分析具有CCD和相邻 lncRNA 缺失等位基因的转基因小鼠.
在新生儿和成人骨肌中评估Igf2表达水平.
多模式染色体分析以确定调节元素和染色体域组织.

主要成果:

删除CCD证实了其作为新生儿肌肉特异性的母体Igf2抑制剂的作用.
删除相邻的lncRNA并没有显著影响Igf2水平.
缺少CCD导致成年骨肌中Igf2的高水平双激活,而在成年骨肌中Igf2通常被抑制.
在ICR和CCD之间发现一种新型的成人骨肌增强剂 (PaSME).

结论:

中央保护域 (CCD) 作为Igf2的发育性,双基性,肌肉特异性抑制剂.
消除CCD使PaSME增强剂能够在成年骨肌中驱动异常的Igf2激活.
这项研究揭示了Igf2/H19位点的新结构调节机制,涉及CCD和PASME.

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