Fig 2: Effects of transcription inhibition by α-amanitin and rpb1 knock-down.a, RPB1 ChIP-seq signal across genes normalized to spike-in K562. b, RPB1 ChIP-seq signal across human genes in spike-in K562 cells. For a & b, Wild type (wt), morpholino control (ctrl), rpb1 morpholino knock-down (rpb1 kd), rpb1 rescue (rpb1 rsc), all experiments were conducted in two biological replicates. c, Effect of transcription inhibition on embryo development. Transcription inhibition with α-amanitin was repeated for at least two times with similar results. d, Arrowhead corner score distribution. e, TAD size distribution. f, Percentage of genome folds in TADs.

Fig 3: Effects of rpb1 knock-down on TAD establishment.a, Effect of rpb1 knock-down on embryo development. Knock-down of rpb1 was repeated for at least two times with similar results. b, Arrowhead corner score distribution. c, TAD size distribution. d, Percentage of genome folds in TADs.

Fig 4: Tissue-specific genome architecture in mature brain, liver and sperm cells.a, Heatmaps of chromosome 2 plotted at a 50-kb resolution for brain and liver cells. b, Hi-C matrices (oberved/expected) and Cscore for chromosome 2 at 50-kb resolution for brain and liver cells. c, Heatmaps of an example region in chromosome 2 showing the gain and loss of TAD structures in the brain, liver and sperm cells compared to s13. The single asterisk next to Liver indicates repeated Hi-C on liver cells with K562 as the spike-in control. d, Aggregated TADs of brain, liver and s13 embryo cells and normalization of aggregated TADs against s13 embryos. e, DI cluster for TADs of brain and liver cells. In brain cells, we identified 874, 3,361 and 912 TADs in clusters 1, 2 and 3, respectively. In liver cells, we identified 11, 2,469 and 5 TADs in clusters 1, 2 and 3, respectively. f, Western blot of CTCF, Rad21, SNF2H, RPB1 and histone H3 as a control in brain and liver cells. The western blot experiments in this figure were repeated at least twice with similar results. g, Heatmap of chromosome 2 plotted at a 50-kb resolution for mature sperm cells.Source data

Fig 5: JAK3 interacts with RNA Polymerase II in MyLa cells. (a) Immunoblots after co-immunoprecipitation assay shows JAK3 interacts with POLR2A in MyLa 2000 (up) and MyLa 2059 (down). (b) Autoradiograph shows in vitro tyrosine phosphorylation of recombinant human Histone H3 by recombinant human JAK3 (left) and the phosphorylation is inhibited by pre-incubating the kinase, JAK3, with 100 nM JAK inhibitor Tofacitinib citrate (JAKi) for 30 min (right side panel). Coomassie staining of the gel shows Histone H3 in all the samples. Recombinant human JAK2 is used as a positive control for the kinase assay.