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Updated: Jun 24, 2025

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在心脏发育和生长过程中,对基斯循环的循环控制

Adrian Arrieta¹, Douglas J Chapski¹, Anna Reese¹

¹Department of Anesthesiology & Perioperative Medicine, David Geffen School of Medicine at UCLA, UCLA, Los Angeles, California, USA.

The Journal of biological chemistry

|June 3, 2024

概括

主昼夜基因Bmal1通过调节基因组循环和染色体组织来驱动新生儿心肌细胞的生长. 它的目标,Sik1,在心脏缩期间协调肌细胞生长与基因转录.

科学领域:

心血管生物学心血管生物学
时间生物学时间生物学
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:

产后心脏缩包括心肌细胞的线性退出和对染色体组织的复制独立的基因素周转.
循环时钟振荡影响核细胞占用率和时钟控制的基因表达在各种组织中.
昼夜时钟在对基因轮和心肌细胞基因表达的时间控制中的作用仍然在很大程度上未被探索.

研究的目的:

调查主昼夜转录因子Bmal1 (大脑和肌肉ARNT类蛋白1) 在基因素周转,染色体组织和肌细胞生长中的作用.
阐明Bmal1在调节新生儿心脏缩期间肌细胞特异性基因表达中的功能.
为了确定参与协调心肌细胞生长和缩反应的新型时钟控制基因.

主要方法:

新生小鼠心室肌细胞中的Bmal1敲击.
对肌细胞大小,蛋白质合成和基因转录 (Nppb,Per2,Tcap,Sik1) 的评估.
使用微球菌核酶定量PCR (MNase-qPCR) 进行染色体可访问性分析.
通过代谢标记测量质子周转量.
Sik1和H3.3a的淘汰实验. 这是一次淘汰实验.

主要成果:

在血清或氨酸刺激后,Bmal1敲击降低了肌细胞大小,蛋白质合成和Nppb转录.
Bmal1 枯竭损害了Per2 和Sik1 的促进子可访问性,并减少了基因素的循环.
Sik1 knockdown 降低了肌细胞大小,抑制了 Nppb 转录,并激活了 Per2 转录.
基因素变异H3.3a的消耗抑制了缩和基诱导的时钟控制的基因转录变化.

结论:

Bmal1对于新生儿心肌细胞生长,复制独立的基因素周转以及Sik1促进体的染色质组织至关重要.
Sik1是一种新型的时钟控制基因,它协调肌细胞生长与多变性和时钟控制的基因转录.
在生长刺激过程中,复制独立的基因组循环对于心脏肌细胞中时钟控制基因的转录重塑至关重要.

关键词:

在这种情况下,染色染色素基因组基因组基因组肌细胞细胞质细胞.核子组中的核子蛋白质稳定症是一种蛋白质稳定症.

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