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. 2020 Apr 10;6(15):eaax5150. doi: 10.1126/sciadv.aax5150

Fig. 4. Hdac1 and Hdac2 cooperate to suppress cryptic transcription through deacetylation of key histone residues at alternative transcription start sites during mammalian cardiogenesis.

Fig. 4

(A and B) H3K23ac (A) and H4K16 (B) staining on Nkx2.5;1KO2KO and 1FF2FF E10.5 sagittal sections at AVC level with cardiac troponin (cTnT) and Hoechst counterstains. Grayscale images are unedited. (C to E) ChIP-qPCR showing relative enrichment (TSSA versus TSSC) of Hdac1and Hdac2 at CS TSSA (C) and Ndufb9 TSSA1 (D), TSSA2 (E), normalized to immunoglobulin G (IgG). (F to I) H3K36me3 (E), H3K23ac (F), H3K14ac (G), and H4K16ac (H) ChIP-qPCR showing relative enrichment over TSSC/TSSAs for CS and Ndufb9 in Nkx2.5;1KO2KO and 1FF2FF E10.5 PHTs. (J) Hdac1/Hdac2 controls cardiomyocyte development at a critical metabolic checkpoint. CHD, chromodomain containing subunit. WT, wild type.