Fig. 5: Promoter bivalency regulates intercellular communication in GI development.

a Aggregate profiles and chromatin state plots, as in Fig. 1f, for genes whose differential expression between Int and St is altered upon PRC2-knockout (as described in Fig. 2a, b). Gene promoters were classified based on their DEG status between control Int and St. Simplified chromatin state maps are shown for E14.5 for both St and Int. b Log2 Fold Change of control stomach-enriched (red) and intestine-enriched (blue) genes upon PRC2 loss in each organ, clustered by degree of H3K27me3 at the promoter (as in Fig. 1f). Box and whisker plots show median (center), 1st and 3rd quartiles (limits of box). Whiskers extended to largest value within 1.5* the interquartile range (defined by box). c, d Tracks overlaying transcription and chromatin accessibility of Wnt2 in the intestinal mesenchyme (c) and Hoxa10 in the stomach mesenchyme (d) in E13.5 control and PRC2-knockout mice. ENCODE ChIP-seq data for H3K27me3 and H3K4me3 (E14.5 and E16.5) and RNA-seq (E16.5) are shown for the respective tissues. e ChIP-qPCR of H3K27me3 and H3K4me3 in mesenchymal cells enriched from E16.5 mice. Multiplicity adjusted p-values were calculated by two-way ANOVA with Bonferroni post-tests (n = 3 biologically distinct sets of embryos, 8 embryos per litter were pooled for each n, ±SEM, *P < 0.05). Source data are provided as a source data file.