About Enhancer
| Enhancer ID: | E_02_0525 |
| Species: | human |
| Position : | chr13:30108722-30109111   |
| Biosample name: | |
| Experiment class : | Low+High throughput |
| Enhancer type: | Enhancer |
| Disease: | -- |
| Pubmed ID: | 30017589 |
| Enhancer experiment: | ChIP-seq |
| Enhancer experiment description: | Our findings were corroborated by H3K4me1 and H3K27ac ChIP-seq data from an alternative na?ve-to-formative differentiation system. As a control, we found little change in these marks at SMC1 sites common to both states. These results indicate that GRHL2 binding correlates with full enhancer activation, suggesting a role for GRHL2 not only in regulation of cohesin binding, but also in regulation of other crucial steps in enhancer activation.Together, these results suggest that our SMC1 ChIP-seq data reflect changing enhancer activity and that cohesin binding at enhancers is highly dynamic during the ESC to EpiLC transition. |
About Target gene
| Target gene : | Dsp(2300002E22Rik,5730453H04Rik,AA407887,AA407888,AW109828,DP,rul),Dsp(2300002E22Rik,5730453H04Rik,AA407887,AA407888,AW109828,DP,rul),Dsp(2300002E22Rik,5730453H04Rik,AA407887,AA407888,AW109828,DP,rul),Dsp(2300002E22Rik,5730453H04Rik,AA407887,AA407888,AW109828,DP,rul) |
| Strong evidence: | CRISPR/Cas9 |
| Less strong evidence: | ChIP-seq,qRT-PCR |
| Target gene experiment description: | We then assessed the effects of each Enhancer deletion on Dsp expression in ES cells and EpiLCs by qRT-PCR.Indeed, we found that deletion of one or both KLF4-bound enhancers led to a significant reduction in Dsp expression in ESCs but had no effect in EpiLCs(Figure 6B). Conversely, deletion of the GRHL2-bound enhancer resulted in significantly reduced Dsp expression in the EpiLC state but had no effect in ESCs (Figure 6B). We observed similar state-specific reductions in target gene expression with deletions of the KLF4-bound and GRHL2-bound enhancers at the Cdh1 and Jam1 loci (Figure 6C and D, S6A and B).;We then assessed the effects of each Enhancer deletion on Dsp expression in ES cells and EpiLCs by qRT-PCR.Indeed, we found that deletion of one or both KLF4-bound enhancers led to a significant reduction in Dsp expression in ESCs but had no effect in EpiLCs(Figure 6B). Conversely, deletion of the GRHL2-bound enhancer resulted in significantly reduced Dsp expression in the EpiLC state but had no effect in ESCs (Figure 6B). We observed similar state-specific reductions in target gene expression with deletions of the KLF4-bound and GRHL2-bound enhancers at the Cdh1 and Jam1 loci (Figure 6C and D, S6A and B).;We then assessed the effects of each Enhancer deletion on Dsp expression in ES cells and EpiLCs by qRT-PCR.Indeed, we found that deletion of one or both KLF4-bound enhancers led to a significant reduction in Dsp expression in ESCs but had no effect in EpiLCs(Figure 6B). Conversely, deletion of the GRHL2-bound enhancer resulted in significantly reduced Dsp expression in the EpiLC state but had no effect in ESCs (Figure 6B). We observed similar state-specific reductions in target gene expression with deletions of the KLF4-bound and GRHL2-bound enhancers at the Cdh1 and Jam1 loci (Figure 6C and D, S6A and B).;We then assessed the effects of each Enhancer deletion on Dsp expression in ES cells and EpiLCs by qRT-PCR.Indeed, we found that deletion of one or both KLF4-bound enhancers led to a significant reduction in Dsp expression in ESCs but had no effect in EpiLCs(Figure 6B). Conversely, deletion of the GRHL2-bound enhancer resulted in significantly reduced Dsp expression in the EpiLC state but had no effect in ESCs (Figure 6B). We observed similar state-specific reductions in target gene expression with deletions of the KLF4-bound and GRHL2-bound enhancers at the Cdh1 and Jam1 loci (Figure 6C and D, S6A and B). |
About TF
| TF name : | Grhl2(0610015A08Rik,BOM,Tcfcp2l3,clft3)Grhl2(0610015A08Rik,BOM,Tcfcp2l3,clft3)Grhl2(0610015A08Rik,BOM,Tcfcp2l3,clft3)Grhl2(0610015A08Rik,BOM,Tcfcp2l3,clft3) |
| TF experiment: | ChIP-seq,ATAC-seq |
| TF experiment description: | Given the strong association between GRHL2 binding and various events in enhancer activation, we asked whether GRHL2 binding is necessary for each of these events. To address this question, we assessed levels of each active enhancer mark in wildtype and GHRL2 KO EpiLCs by performing ATAC-seq and ChIP-seq for H3K4me1, H3K27ac, and SMC1. There was a strong reduction in all active enhancer marks (chromatin accessibility, H3K4me1, H3K27ac, and SMC1 levels) at GRHL2 sites in GRHL2 KO EpiLCs, suggesting a near complete block in enhancer activation in the absence of GRHL2. Together, these results indicate an absolute requirement for GRHL2 for enhancer activation specifically at its target sites.;Given the strong association between GRHL2 binding and various events in enhancer activation, we asked whether GRHL2 binding is necessary for each of these events. To address this question, we assessed levels of each active enhancer mark in wildtype and GHRL2 KO EpiLCs by performing ATAC-seq and ChIP-seq for H3K4me1, H3K27ac, and SMC1. There was a strong reduction in all active enhancer marks (chromatin accessibility, H3K4me1, H3K27ac, and SMC1 levels) at GRHL2 sites in GRHL2 KO EpiLCs, suggesting a near complete block in enhancer activation in the absence of GRHL2. Together, these results indicate an absolute requirement for GRHL2 for enhancer activation specifically at its target sites.;Given the strong association between GRHL2 binding and various events in enhancer activation, we asked whether GRHL2 binding is necessary for each of these events. To address this question, we assessed levels of each active enhancer mark in wildtype and GHRL2 KO EpiLCs by performing ATAC-seq and ChIP-seq for H3K4me1, H3K27ac, and SMC1. There was a strong reduction in all active enhancer marks (chromatin accessibility, H3K4me1, H3K27ac, and SMC1 levels) at GRHL2 sites in GRHL2 KO EpiLCs, suggesting a near complete block in enhancer activation in the absence of GRHL2. Together, these results indicate an absolute requirement for GRHL2 for enhancer activation specifically at its target sites.;Given the strong association between GRHL2 binding and various events in enhancer activation, we asked whether GRHL2 binding is necessary for each of these events. To address this question, we assessed levels of each active enhancer mark in wildtype and GHRL2 KO EpiLCs by performing ATAC-seq and ChIP-seq for H3K4me1, H3K27ac, and SMC1. There was a strong reduction in all active enhancer marks (chromatin accessibility, H3K4me1, H3K27ac, and SMC1 levels) at GRHL2 sites in GRHL2 KO EpiLCs, suggesting a near complete block in enhancer activation in the absence of GRHL2. Together, these results indicate an absolute requirement for GRHL2 for enhancer activation specifically at its target sites. |
About Function
| Enhancer function : | GRHL2 therefore control over a subset of the naive network via Enhancer switching to maintain expression of epithelial genes upon exit from naive pluripotency |
| Enhancer function experiment: | ChIP-seq |
| Enhancer function experiment description: |
Together,these results suggest that our SMC1 ChIP-seq data reflect changing Enhancer activity and that cohesin binding at Enhancers is highly dynamic during the ESC to EpiLC transition. |
About SNP
| SNP ID: | -- |
Upstream Pathway Annotation of TF
| GeneName | Pathway Name | Source | Gene Number |
|---|
Enhancer associated network
The number on yellow line represents the distance between enhancer and
target gene