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在氨基酸限制下,协调的基因组甲基化损失和MYC激活促进了转化能力

Chen Cheng¹, Trent Su¹, Marco Morselli^2,3

¹Department of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles, CA, 90095, USA.

Cancer & metabolism

|June 16, 2025

概括

细胞通过改变色素来适应氨基酸缺乏,特别是减少H4K20me1并增加MYC. 这促进了蛋白质合成,以便在营养物质充足后快速恢复.

科学领域:

细胞生物学细胞生物学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
分子生物学分子生物学

背景情况:

细胞通过信号和表观遗传机制适应营养的波动.
氨基酸 (AA) 缺乏通过mTORC1无活化抑制蛋白质合成.
在AA限制期间支持细胞适应和恢复的表观遗传途径尚不清楚.

研究的目的:

调查在AA限制期间染色体和转录性变化如何保持翻译能力.
了解细胞如何在AA补充后为生长做准备.

主要方法:

在AA补充/贫乏条件下培养的人类细胞.
通过Westernblotting和ChIP-seq.评估了全球基因素甲基化 (H4K20me1).
评估基因表达和转录输出使用RNA-seq和chromRNA-seq.
通过核糖体分析和OPP合并试验测量蛋白质合成.
通过敲击/过度表达测试了SETD8和MYC的功能贡献.

主要成果:

缺少AA导致全基因组的H4K20me1丢失,并增加MYC表达,特别是在核糖体蛋白和转化因子的基因中.
细胞在AA限制期间表现出增加的翻译能力,在补充后的翻译增强.
H4K20me1的丢失是独立于mTORC1的,部分是由SETD8的下调驱动的.
结合SETD8敲除和MYC过度表达诱导了翻译相关基因和增强的蛋白质合成.

结论:

一个基于色素的机制将代谢状态与转录调节相结合,以适应AA限制.
H4K20me1的损失和MYC活动的增加在AA剥夺期间为快速恢复提供了转化机制.
这种机制有助于在营养物质波动下竞争性增长,并对MYC驱动的癌症产生影响.

关键词:

氨基酸限制的限制癌症癌症癌症癌症表观遗传适应表观遗传适应 H4K20me1 在线观看基质子的修改基质子的修改我的世界 MYC 翻译能力的提高

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