Genome-wide occupanies of Ssu72, Pol II, pSer2, pSer5, pSer7 and pThr4 of Ssu72 Wild Type and Knock-out MEFs and hepatocytes

We report the genome-wide occupanies for high-throughput profiling of Pol II and Pol II CTD phosphorylation modifications in mammalian cells and tissues. By obtaining over three billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of mouse embryonic stem cells, embryonic fibroblasts and primary hepatocytes. Loss of mammalian Ssu72 was found to be related to defect of transcriptional elongation though the defects of Pol II CTD phophorylational dynamics. In addition, depletion of Ssu72 resulted in defects of Pol II elongation by reducing CTD Ser2 and Thr4 phosphorylation which induced Pol II accumulation at the proximal promoter region by increasing CTD Ser5 and Ser7 phosphorylation of transcriptionally active genes in a tissue-specific manner. Our results revealed a fundamental role of mammalian Ssu72 in regulating RNA Pol II-mediated transcriptional plasticity for cell-type-specific homeostatic maintenance. Examination of Ssu72, Pol II and CTD modifications in 3 cell types.