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. 2023 Nov 29;624(7991):433–441. doi: 10.1038/s41586-023-06793-z

Extended Data Fig. 4. FoxP3 can bridge TnG repeat-containing sites in vivo.

Extended Data Fig. 4

a-c. Comparison of (a) H3K4me3-ChIP, (b) ATAC and (c) H3K27ac-ChIP signal23 around the CNR union peaks with and without TnG repeat-like sequences in pre-thymic Tregs (pre-tTregs) and thymic Tregs (tTregs) (n = 3,301 peaks and 5,761 peaks, respectively). Right: ChIP/ATAC signal was averaged over +/− 500 bp around the CNR peak summits. Two-tailed unpaired t-tests. ****, p < 0.0001. d. FoxP3-dependence of the chromatin contacts at FoxP3-bound TnG anchors in Fig. 2f. FoxP3-bound TnG anchors were defined as anchors that overlap with FoxP3 CNR peaks with TnG repeat-like sequences. Contacts with frequency>5 in WT Treg HiC and connected by two TnG anchors were analysed with an increasing FoxP3 PLAC-seq count threshold. For each contact, log2 foldchange of HiC counts from WT to FoxP3 knock-out Treg were plotted. Contacts with FDR < 10 were coloured red. The majority of the TnG–TnG contacts were less frequent in FoxP3 knock-out than in WT Tregs, although smaller fractions (10-15%) showed statistically significant FoxP3 dependence (FDR < 10), as previously reported12. n = 4365, 2559, 813, 204 and 60 anchors respectively. Mean ± SD were shown in black and blue lines. See also Supplementary Table 3. e. Fraction of the FoxP3-bound TnG anchors from Fig. 2f that overlap with previously published Treg EPL anchors13.