H3K18和H3K23乙化指导建立MLL介导的H3K4甲基化
Geoffrey C Fox1, Karl F Poncha2, B Rutledge Smith3
1Curriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill, School of Medicine, Chapel Hill, NC.
bioRxiv : the preprint server for biology
|May 27, 2024
概括
在H3K18和H3K23的基因组乙化特别刺激了MLL1和MLL4复合体的H3K4甲基化. 这一发现解释了基因素乙化和活性基因表达之间的联系.
科学领域:
- 表观遗传学和基因调控
- 染色体生物学 染色体生物学
- 转录的分子机制的转录
背景情况:
- 基因组N端尾与DNA相互作用,限制了对DNA和修饰部位的访问.
- 希斯乙化中和了电荷,破坏了DNA-尾巴相互作用,并促进了残留物进入.
- 之前的研究发现了MLL1.1对H3K4三甲基化 (H3K4me3) 的聚乙化介导的染色质开关.
结论:
- H3K18和H3K23的乙化独特而强烈地刺激了H3K4的甲基化.
- 提供了关于基因素乙化和活性基因表达之间的关联的见解.
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