交易激励
生物
组蛋白
发起人
甲基化
组蛋白H3
转录因子
染色质
DNA甲基化
细胞生物学
感光细胞
基因表达
基因表达调控
视网膜
遗传学
基因
神经科学
作者
Xixiang Zhang,Bowen Zhang,Lue Xiang,Hui Wu,SUPIT Alva Sahiri Alexander,Peipei Zhou,Melvin Zi-Yu Dai,Xiaoyun Wang,Wenjun Xiong,Yan Zhang,Zi-Bing Jin,Lih-Wen Deng
出处
期刊:iScience
[Elsevier]
日期:2022-03-01
卷期号:25 (4): 104058-104058
被引量:1
标识
DOI:10.1016/j.isci.2022.104058
摘要
Histone methylation, particularly at the H3K4 position, is thought to contribute to the specification of photoreceptor cell fate; however, the mechanisms linking histone methylation with transcription factor transactivation and photoreceptor gene expression have not yet been determined. Here, we demonstrate that MLL5 is abundantly expressed in the mouse retina. Mll5 deficiency impaired electroretinogram responses, alongside attenuated expression of a number of retina genes. Mechanistic studies revealed that MLL5 interacts with the retina-specific transcription factor, CRX, contributing to its binding to photoreceptor-specific gene promoters. Moreover, depletion of MLL5 impairs H3K4 methylation and H3K79 methylation, which subsequently compromises CRX-CBP assembly and H3 acetylation on photoreceptor promoters. Our data support a scenario in which recognition of H3K4 methylation by MLL5 is required for photoreceptor-specific gene transcription through maintaining a permissive chromatin state and proper CRX-CBP recruitment at promoter sites.
科研通智能强力驱动
Strongly Powered by AbleSci AI