Fig. 7
From: An enhancer cluster controls gene activity and topology of the SCN5A-SCN10A locus in vivo
Regulatory function of RE6-9 is partially compensated during development. a Analysis of Scn5a+/Δ7 and RE6-9+/− embryos at E10.5. Heterozygous Scn5a and RE6-9 mutants develop normally. Compound heterozygous mutants Scn5aΔ7/ΔRE6-9 are lethal at E10.5 and are phenotypically similar to Scn5aΔ7/Δ7. b RE6-9−/− embryos at E13.5 reveals embryonic lethality. c RE6-8−/− embryos at E13.5 develop normal and do not show cardiac defects. White scale bars are all 1 mm. d, e Absolute expression level of Exog, Scn5a, Scn10a, and Wdr48 of E10.5 whole heart RE6-9−/− embryos (d) and E13.5 whole heart RE6-8−/− embryos (e) compared to wildtype (WT). f, g Fold change expression level of Exog, Scn5a, Scn10a, and Wdr48 of E10.5 whole heart RE6-9−/− embryos (f) and E13.5 whole heart RE6-8−/− embryos (g). Bars represent mean ± SEM and P values were calculated using one-way ANOVA with post hoc Bonferroni tests. WT n = 4; RE6-9+/− n = 5; RE6-9−/− n = 5; WT n = 5; RE6-8+/− n = 5; RE6-8−/− n = 7. **P < 0.01, ***P < 0.001. h UCSC browser view of the enhancer cluster RE6-9 showing H3K27ac ChIP41 at different stage of pre- and postnatal heart. Source data are provided as a Source Data file
