Extended Data Fig. 7: INTS12 phosphorylation and the Integrator’s endonuclease activity are required for establishing UV-induced Pol II elongation wave.
From: Integrator subunit INTS12 links ribotoxic stress to transcription-coupled nucleotide excision repair
a, Heatmaps of Pol II ChIP-Rx signals across gene body regions in control cells after mock or different doses of UV treatment, followed by 1 h recovery. Genes were ranked by decreasing Pol II occupancy under mock treatment conditions. FC, fold change. b, Heatmaps of Pol II ChIP-seq signals across gene body regions in CSB KO cells after mock or UV treatment, followed by recovery for the indicated times. Genes were ranked by decreasing Pol II occupancy under mock treatment conditions. FC, fold change. c, Metaplots of Pol II ChIP-seq signals across gene body regions in CSB KO cells after mock or UV treatment, followed by recovery for the indicated times. d, Schematic illustrating the preDRB-nRNA-seq. Cells released from DRB pretreatment were labeled with 4-SU at the indicated times after recovery from UV irradiation. e, Heatmaps of the Pol II ChIP-Rx signals across gene body regions in INTS12 KO cells reconstituted with stably expressed WT INTS12-Flag after mock treatment or UV treatment, followed by recovery for the indicated times. Genes were ranked by decreasing Pol II occupancy under mock treatment conditions. FC, fold change. f, Metaplots of Pol II ChIP-Rx signals across gene body regions in INTS12-WT cells after mock or UV treatment, followed by recovery for the indicated times. g, Heatmaps of the Pol II ChIP-Rx signals across gene body regions in INTS12 KO cells reconstituted with stably expressed WT INTS12-Flag after mock treatment or UV treatment, followed by recovery for the indicated times. Genes were ranked by decreasing Pol II occupancy under mock treatment conditions. FC, fold change. h, Metaplots of Pol II ChIP-Rx signals across gene body regions in INTS12-3A cells after mock or UV treatment, followed by recovery for the indicated times. i, Cumulative distribution of PSI in INTS12 KO cells reconstituted with stably expressed WT or 3 A INTS12-Flag. j, Lysates from parental or INTS11-dTAG DLD1 cells treated with indicated chemicals were analyzed by WB. k, l, Heatmaps of Pol II ChIP-Rx signals across gene body regions in DMSO (k) or dTAG (l) treated INTS11-dTAG DLD1 cells after mock or UV treatment, followed by recovery for the indicated times. Genes were ranked by decreasing Pol II occupancy under mock treatment conditions. FC, fold change. m, n, Metaplots of Pol II ChIP-Rx signals across gene body regions in DMSO (m) or dTAG (n) treated INTS11-dTAG DLD1 cells after mock or UV treatment, followed by recovery for the indicated times.
