Fig. 6: Analysis of SMAD4 binding in endometrial organoids reveals differential binding across the genome.
From: SMAD2/3 signaling in the uterine epithelium controls endometrial cell homeostasis and regeneration
a Diagram outlining the procedures used to identify SMAD4-bound genes in organoids from Control and Smad2/3 cKO mice using CUT & RUN. b Heatplot showing the SMAD4 signal distribution across the transcriptional start site (TSS) and transcriptional end site (TES) in Control and Smad2/3 cKO organoids. As expected, the SMAD4 signal in the Smad2/3 cKO organoids was decreased when compared to the SMAD4 signal in Control organoids. c Feature distribution comparison between the SMAD4 binding sites in Control and Smad2/3 cKO organoids. d Motif sequence analyses in the SMAD4-bound regions in Control and Smad2/3 cKO organoids. e Differentially bound SMAD4 genes in Control (representing SMAD2/3 targets) and Smad2/3 cKO organoids (representing SMAD1/5 targets) and the gene ontology analysis of the differentially bound genes in Control organoids. f Genome track screenshot showing increased SMAD4 enrichment in the upstream promoter region of the BMP-target gene, Id3, in Smad2/3 cKO organoids when compared to Control organoids. CUT & RUN experiments were performed in the organoids from >3 mice per genotype, analyzed and sequenced as duplicates.
