期刊
MOLECULAR CELL
卷 39, 期 5, 页码 750-760出版社
CELL PRESS
DOI: 10.1016/j.molcel.2010.08.010
关键词
-
资金
- European Union
- German Research Council
Activation of transcription from a silenced state is crucial to achieve specific gene expression in many biological contexts. Methylation of lysine 9 on histone H3 (H3K9) is widely associated with transcriptional silencing, and its disappearance is linked to the activation of several inflammatory genes by NF-kappa B. Here we describe that this event is controlled by a feed-forward circuit catalyzed by the activity of the histone demethylase Aof1 (also known as Lsd2/Kdm1b). We find that Aof1 is required for removal of dimethyl H3K9 at specific promoters, and thereby it controls stimulus-induced recruitment of NF-kappa B and gene expression. However, Aof1 is itself recruited by interaction with the c-Rel subunit of NF-kappa B, which is found at low levels associated with promoters in unstimulated cells. Thus, at these tightly regulated genes, NF-kappa B functions both as a transcriptional activator and as an upstream targeting signal that marks promoters to be derepressed by histone demethylation.
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