Npac_ChIPSeq

Though chromatin modification makes great contribution to pluripotency maintenance in embryonic stem cell (ESC), it remains obscure for the mechanisms. Here, we show that one "reader" of histone H3 trimethyl lysine 36 (H3K36me3), Npac, is essential to maintain mouse ESC pluripotency. On one hand, depletion of Npac causes mESC differentiation by repressing genes associated with pluripotency while activating developmental-related genes. On the other hand, depletion of Npac inhibits reprogramming efficiency. Further, ChIP-seq reveals that Npac co-localizes with H3K36me3 in the gene bodies of active genes in mouse ES cells. In addition, we find Npac interacts with P-TEFb, RNA Pol II Ser2 and Ser5, depletion of Npac results in the transcriptional elongation defect at pluripotency genes Nanog and Rif1. Thus, we propose that Npac activates pluripotency-associated gene expression by recruiting of P-TEFb and interacting with RNA Pol II Ser2 and Ser5, further promotes productive transcriptional elongation. Examination of Npac-binding sites in mouse embryonic stem cells.