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. 2017 Oct 12;9(5):1516–1529. doi: 10.1016/j.stemcr.2017.09.011

Figure 2.

Figure 2

Changes in H3K9ac and H3K9me3 at Bivalently Marked Promoters

(A) Biological processes of genes with bivalent promoters were determined by gene ontology analysis. Pertinent biological process and associated binomial p values are listed.

(B) A consensus logo plot for NEUROG1 binding site containing an E-box (CANNTG).

(C) ChIP-seq peaks for POLR2A, H3K4me3, and H3K27me27 for Cdk2. Arrowheads indicate the approximate location of primers used for ChIP-qPCR. The number indicates the relative base-pair distance from the TSS.

(D) Enrichment of H3K9ac (active) or H3K9me3 (repressive) marks at the Cdk2 promoter region by ChIP-qPCR in proliferating iMOP (n = 3) and iMOP-derived neurons (n = 3). Background levels were determined by performing ChIP-qPCR with non-specific rabbit IgG control antibody.

(E) ChIP-seq peaks for POLR2A, H3K4me3, and H3K27me27 at NeuroD1. Arrowheads indicate the approximate location of primers relative to the TSS used for ChIP-qPCR.

(F) ChIP-qPCR of H3K9ac and H3K9me3 at the NeuroD1 promoter in proliferating progenitor (n = 3) and iMOP-derived neurons (n = 3).

(G) ChIP-seq peaks for POLR2A, H3K4me3, and H3K27me27 at Pou5f1.

(H) ChIP-qPCR of H3K9ac and H3K9me3 at the Pou5f1 promoter in proliferating progenitors (n = 3) and iMOP-derived neurons (n = 3).

Error bars denote ±SEM. ∗∗p < 0.01, ∗∗∗p < 0.001.