Extended Data Fig. 5: INTS12 and its phosphorylation facilitate DNA repair by TC-NER following UV irradiation.
From: Integrator subunit INTS12 links ribotoxic stress to transcription-coupled nucleotide excision repair
a, qRT-PCR analysis of the mRNA levels of XPC in the indicated cells. The error bars indicate mean ± s.d. with n = 3 biologically independent samples. b, Unscheduled DNA synthesis in mock or UV-irradiated XPC-deficient cells that were either untreated or treated by ZAKi (1 µM, pre-1h) were analyzed by EdU labeling. Right: Quantification of relative EdU levels per cell (n = 128, 128, 121, 123). Red lines indicate the mean intensity in each group. Scale bar, 50 μm. c, Metaplots of XR-seq signal across gene body regions for nonoverlapping protein-coding genes in DMSO- or ZAKi-treated cells after UV treatment. d, Relative quantification of TCR activity based on the ratio of XR-seq read counts from TSs and NTSs in expressed protein-coding genes (n = 3901, TPM > 5). P < 7.03E-298. e, Metaplots showing the average level of TCR-seq signals from the TSS until the TTS (−2 kb and +2 kb, respectively) in control or INTS12 KO cells after mock or UV treatment, followed by recovery for the indicated times. f, Genome browser tracks showing the strand-specific TCR-seq read distribution across the representative gene in mock- or UV-irradiated control and INTS12-KO cells. g, Time course analysis of the recovery index (RI) in control and INTS12-KO cells following UV irradiation to estimate TC-NER kinetics on a global scale. h, Strand-specificity index (SSI) scatterplots derived from TCR-seq signals of allexpressed genes in control or INTS12 KO cells after mock or UV treatment, followed by recovery for the indicated times. Statistical analysis was performed using two-tailed unpaired t-tests.
