Fig 4. ARID1A-dependent OCRs in d8 MP, EEC, and TE cells are largely shared across subsets.

WT, Arid1a^cKO and Arid1a^cHet effector cells were isolated at d8 p.i. and sorted based on expression of TE, EEC and MP markers as defined in Figure 3A and differential OCRs were compared by ATAC-sequencing (2-fold change, adjusted p value<0.05, Benjamini-Hochberg). (A) Principal component analysis plot of ATAC-seq from WT, Arid1a^cHet, and Arid1a^cKO subsets at d8 post-infection. (B) Number of OCRs lost and gained in Arid1a^cKO and Arid1a^cHet subsets relative to WT cells. (C-D) ATAC-seq signal heatmaps of WT, Arid1a^cHet, and Arid1a^cKO d8 subsets. OCRs are clustered by whether they are lost in the Arid1a^cKO relative to WT cells in individual subsets or lost in all three subsets (C) and UpSet plot shows the number of shared and subset-specific OCRs lost in Arid1a^cKO subsets relative to WT cells (D). (E) Gene expression and paired chromatin accessibility of annotated OCRs in Arid1a^cKO and WT d8 subsets. TE- and MP-signature genes are highlighted in blue and red, respectively. (F) H3K27ac CUT&RUN signal coverage centered on ARID1A-dependent ATAC-seq peaks in WT vs. Arid1a^cKO cells TE, EEC, and MP cells.