Extended Data Fig. 6: Loss of the L1 domain of TCF-1 has limited effect on chromatin accessibility in committed T cells.

a) Principal component plot of RNA-seq on Tcf7^−/− DN3 like Scid.adh cells transduced with empty vector (EV), wild type (WT) TCF-1, and internal deletion mutants: ΔL1, ΔL2, ΔL6, and ΔL7. b) Volcano plot demonstrating significantly differential genes comparing WT TCF-1 and EV (left), ΔL1 and WT TCF-1 (middle), and ΔL7 and WT TCF-1 (right) transduced Tcf7^−/− DN3 cells. (adjusted P<0.05 and |Log2FoldChange|>1) P-values are calculated by the Wald test and adjusted using the Benjamini and Hochberg method. c) Heatmap depicting significantly up and down-regulated genes comparing WT TCF-1 and EV transduced Tcf7^−/− DN3 cells. (adjusted P <0.05 and |Log2FC|>1). P-values are calculated by the Wald test and adjusted using the Benjamini and Hochberg method. d) Pathway enrichment analysis of differential gene sets depicted in B. P values are calculated using a hypergeometric test. e) Quantification of number of WT TCF-1 and ΔL1 binding events profiled by TCF-1 and FLAG CUT&RUN in Tcf7^−/− KO DN3 cells. Bars represent mean number of binding sites from n = 2 biologically independent samples. f) Principal component plot of WT TCF-1 and ΔL1 binding events as measured in E.