Fig. 4

The remodeled nr2f1a mutant SV acquires characteristics of the arterial BA.

a Schematic depicting the dissection of individual cardiac chambers for single cell RNA-seq analysis. b Uniform Manifold Approximation and Projection (UMAP) plot showing the 15 ICGS2 clusters corresponding to smooth muscle, endothelial, and epithelial cells. asm – arterial smooth muscle, vsm – venous smooth muscle, psml – pan-smooth muscle-like, vlec – venous-lymphatic endothelial cell, aec – arterial endothelial cell, ecp – endothelial cell progenitor, epi – epithelial cell. c The UMAP plot shows the contributions of cells from each the WT BA, WT SV, nr2f1a^aco mutant BA, and nr2f1a^aco mutant SV. Dashed outlines indicate cells from clusters 1, 7, and 10 (SMCs) and clusters 9 and 10 (ECs) occupying similar space that are from the WT BA, WT SV, and nr2f1a^aco mutant SV. d Dot matrix plot comparing the expression of selected SMC and ECs marker genes within clusters 1–13. e Gene-enrichment (GO-Elite) of WT cluster marker genes compared to previously published arterial, venous, and intermediate vascular populations. f GO enrichment of marker genes from nr2f1a^aco mutant C6 vs WT C6 SMC populations. Gene-set enrichment analysis is performed using GO-Elite. A Z-score and Fisher’s Exact two-sided Test p-value are calculated to assess over-representation of Ontology terms, gene-sets, and pathways. Adjusted p-values (FDR p-values) for these various tests are calculated using the Benjamini-Hochberg correction method. g Frequency of cells from clusters in the nr2f1a^aco mutant and WT SV. h Frequency of cells from clusters in the nr2f1a^aco mutant and WT BA. i Pseudotime analysis was performed with Monocle2 mapping cellular identities from the SMC clusters (1–8). j Individual 10x Genomics captures showing separated populations from (i). Dashed outline indicates nr2f1a^aco mutant SV cells occupying trajectories that are normally found almost exclusively in the WT and nr2f1a^aco mutant BA.