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信号塑造了H3K27ac和H3K18la的代谢控制,以调节EGA

Virginia Savy¹, Paula Stein¹, Don Delker²

¹Reproductive Medicine Group, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.

bioRxiv : the preprint server for biology

|March 31, 2025

概括

在受精时过量的 (Ca2+) 通过改变新陈代谢和表观遗传标记来破坏胚胎发育和后代健康. 恢复乳基CoA水平挽救了这些效应,揭示了Ca2+动态.

科学领域:

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

背景情况:

辅助生殖技术 (ART) 增加后代的代谢风险,其机制尚不清楚.
(Ca2+) 信号启动胚胎发育,但在ART中被破坏.
在小鼠胚胎中异常的Ca2+会损害发育和成人代谢.

研究的目的:

研究将受精时的Ca2+动态与胚胎发育和后代健康联系起来的机制.
确定改变的Ca2+如何影响代谢基质的可用性和表观遗传重编程.
确定潜在的干预措施,以减轻与ART相关的风险.

主要方法:

使用基因小鼠模型和ionomycin治疗来操纵受精卵中的细胞内Ca2 +.
使用超低输入CUT&Tag.使用分析的表观遗传修饰 (H3K27ac,H3K18la).
评估了全球转录和代谢基质水平 (乙-CoA,乳-CoA).

主要成果:

在受精时增加的Ca2+改变了H3K27ac和H3K18la水平,并减少了全球转录.
过多的Ca2+增加了pyruvate脱酶的活性,并降低了乳酸盐水平.
补充乳基CoA恢复了表观遗传标记和转录,拯救了发育效应.

结论:

Ca2+动态是代谢基质可用性和受精期间表观遗传重编程的关键调节者.
由ART引起的Ca2+干扰会导致表观遗传标记改变和胚胎发育受损.
针对乳基CoA的代谢干预可以提供一种改善ART结果的策略.

关键词:

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