染色质
PRC2
核糖核酸
染色质免疫沉淀
异染色质
生物
核糖核酸酶P
细胞生物学
芯片排序
芯片对芯片
DNA
遗传学
染色质重塑
计算生物学
EZH2型
基因表达
基因
发起人
作者
Evan Healy,Qi Zhang,Emma H Gail,Samuel C. Agius,Guizhi Sun,Michael Bullen,Varun Pandey,Partha Pratim Das,José M. Polo,Chen Davidovich
出处
期刊:Cell Reports
[Elsevier]
日期:2024-03-01
卷期号:43 (3): 113858-113858
被引量:2
标识
DOI:10.1016/j.celrep.2024.113858
摘要
Summary
RNA has been implicated in the recruitment of chromatin modifiers, and previous studies have provided evidence in favor and against this idea. RNase treatment of chromatin is commonly used to study RNA-mediated regulation of chromatin modifiers, but the limitations of this approach remain unclear. RNase A treatment during chromatin immunoprecipitation (ChIP) reduces chromatin occupancy of the H3K27me3 methyltransferase Polycomb repressive complex 2 (PRC2). This led to suggestions of an "RNA bridge" between PRC2 and chromatin. Here, we show that RNase A treatment during ChIP causes the apparent loss of all facultative heterochromatin, including both PRC2 and H3K27me3 genome-wide. We track this observation to a gain of DNA from non-targeted chromatin, sequenced at the expense of DNA from facultative heterochromatin, which reduces ChIP signals. Our results emphasize substantial limitations in using RNase A treatment for mapping RNA-dependent chromatin occupancy and invalidate conclusions that were previously established for PRC2 based on this assay.
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