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. Author manuscript; available in PMC: 2011 Feb 1.
Published in final edited form as: Curr Opin Neurobiol. 2010 Feb;20(1):29–36. doi: 10.1016/j.conb.2010.01.003

Figure 2.

Figure 2

Regulation of neural cell fate specification by histone methylation and demethylation.

(A) Trimethylation (3me, red dots) of H3-K9 and H3-K27 are hallmarks of a condensed/transcriptionally repressed chromatin state, whereas trimethylation of H3-K4 (H3K4me3) marks transcriptionally active chromatin.

(B) In neural progenitors, the promoter of GFAP, an astrocytes-specific marker gene, exhibits high level of H3K9me3, transcriptionally repressive chromatin mark. FGF2 signal removes H3K9me3 and triggers H3K4me3, transcriptionally active chromatin mark, on the GFAP promoter. This facilitates access of the STAT-CBP complex to the STAT-response element (SRE) in the GFAP promoter upon CNTF signal, leading to efficient differentiation of neural progenitors to astrocytes.

(C) MLL1, a H3-K4 methyltransferase, is recruited to the promoter of Dlx2 by an unknown transcription factor (X), and promotes neuronal differentiation as well as Dlx2 expression. In the absence of MLL1, H3K27me3 levels on Dlx2 gene were markedly increased, suppressing Dlx2 expression and neuronal differentiation. The identity of H3-K27 demethylases (H3K27DMs) involved in the removal of H3K27me3 on Dlx2 gene remains unclear.

(D) During the neurogenic-to-astrogenic fate switch of neural progenitors, the chromatin status of the Neurog1 promoter changes from the acetylated open chromatin to the transcriptionally repressive chromatin marked by H3K27me3. These changes are mediated by Polycomb repressor complexes (PRCs).