Enhancers near the c-fos gene with increased CBP/RNAPII/NPAS4 binding and eRNA production upon membrane depolarization
The strong inducibility of CBP binding at thousands of neuronal enhancers and their presence near activity-regulated genes (e.g., c-fos, rgs, and nr4a2) (Fig. 1 and Supplementary table 2) suggests that these enhancers may contribute to the induction of activity-regulated gene expression.
We find in neurons that CREB, SRF, and NPAS4 bind to neuronal enhancers as well as promoters (Supplementary Table 3).
This tight co-localization of individual TFs with CBP at a subset of enhancers (Supplementary Table 4) suggests that TFs may work together to regulate enhancer function, possibly by recruiting CBP.
We provide genome-wide evidence that thousands of neuronal activity-regulated enhancers that are defined by activity-independent H3K4me1 marks and activity-dependent CBP binding also recruit RNAPII and produce eRNAs
http://genome.ucsc.edu/cgi-bin/hgEncodeVocab?term=CTCF,H3K4me1,H3K4me2,H3K4me3,H3K27ac,H3K9ac,H3K36me3,H4K20me1,H3K27me3,Input
| H3K4me1 | Histone H3 (mono methyl K4). Is associated with enhancers, and downstream of transcription starts. |
| H3K4me2 | Histone H3 (di methyl K4). Marks promoters and enhancers. Most CpG islands are marked by H3K4me2 in primary cells. May be associated also with poised promoters. |
| H3K4me3 | Histone H3 (tri methyl K4). Marks promoters that are active or poised to be activated. |
| H3K27ac | Histone H3 (acetyl K27). As with H3K9ac, associated with transcriptional initiation and open chromatin structure. It remains unknown whether acetylation has can have different consequences depending on the specific lysine residue targeted. In general, though, there appears to be high redundancy. Histone acetylation is notable for susceptibility to small molecules and drugs that target histone deacetylases. |
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