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Fig. 7 | Genome Biology

Fig. 7

From: Genome-wide studies reveal the essential and opposite roles of ARID1A in controlling human cardiogenesis and neurogenesis from pluripotent stem cells

Fig. 7

ARID1A interacts with co-factors. a Prediction of co-factors interacting with ARID1A according to transcriptional factor binding motifs in ARID1A ChIP-seq peaks. b Top three transcription factor motifs surrounding ARID1A cis-regulatory binding elements. c Comparison between ARID1A-and REST-occupied gene lists from ChIP-seq datasets. Hypergeometric model was used to calculate the significance of overlap between ARID1A and REST target genes, and p value of enrichment of genes in both ARID1A and REST targets. d, e Comparison between ARID1A- and REST-occupied neural (d) and cardiac genes (e) from ChIP-seq datasets, indicating that REST and ARID1A prefer to co-occupy neural genes than cardiac genes. f Integrative analysis of ARID1A ChIP-seq (1st column), REST ChIP-seq (2nd column), differential chromatin accessibility (DCA) by ATAC-seq (KO vs. WT) (3rd column), and average gene expression levels (GE, log2 (fold change)) from scRNA-seq (KO vs. WT, 4th and 5th columns). Purple boxes (1st column) show the representative ARID1A-occupied genes from d, while green boxes (2nd column) show REST occupancies on those genes. g Same scheme design as f to show ARID1A and REST occupancies on representative cardiogenic genes are shown. h Western blotting to detect temporal protein expressions of REST, T, and MEF2C during cardiac differentiation of hESCs. Protein samples were collected on days 0 (T0), 2 (T2), 3 (T3), 4 (T4), and 6 (T6). i–k Co-IP validation of the interaction between ARID1A and REST in undifferentiated hESCs (T0) (i), the interaction between ARID1A and T in hESCs at day 2 of differentiation (T2) (j), and the interaction between ARID1A and MEF2C in hESCs at day 6 of differentiation (T6) (k). l Schematic summary of ARID1A’s roles in human cardiac and neural commitment from hESCs

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