Extended Data Fig. 7: Chromatin accessibility noise is elevated in high plasticity states of lung adenocarcinoma.
From: Thymic epithelial cells amplify epigenetic noise to promote immune tolerance
a,b, UMAP of merged scATAC-seq data from lung adenocarcinomas44 (LUAD) in p53-KO and p53-WT mice colored by genotype (a) and cluster annotation (b). c–f, LUAD progression depicted by aggregate expression of genes defining alveolar type-2 (AT2) lung epithelial state43 (c), mixed alveolar type-1 and type-2 lung epithelial state43 (d), embryonic liver state43 (e) or epithelial-to-mesenchymal transition (EMT) state43 (f) overlayed on scATAC-seq UMAP from (b). g, Fraction of scATAC-seq fragments within scATAC-seq peaks (WIP) overlayed on UMAP from (b). h, Fraction of mononucleosomal scATAC-seq fragments overlayed on UMAP from (b). i,j, Violin plots depicting WIP fraction (i) or the fraction of mononucleosomal scATAC-seq fragments (j) within cells (n = 3,172: C1 = 612, C2 = 511, C3 = 112, C4 = 581, C5 = 425, C6 = 188, C7 = 190, C8 = 553) across annotated LUAD clusters defined in (b–f). Box plots depict median, 25th and 75th percentile, whiskers represent 1.5 times interquartile range. P-values from one-sided Mann-Whitney U-tests. k, Nkx2-1 gene expression levels overlayed on scATAC-seq UMAP from (b). l, Prevalence of NKX2.1-binding motifs across accessible LUAD genomes (chromVAR deviation scores) overlayed on scATAC-seq UMAP from (b). m, Runx2 expression overlayed on scATAC-seq UMAP from (b). n, Prevalence of RUNX2-binding motifs across accessible LUAD genomes (chromVAR deviation scores) overlayed on scATAC-seq UMAP from (b).
