Mechanisms of transcriptional repression in response to genome stress-role of histone H3 phosphorylation at T11-

在本研究中，我们发现组蛋白H3-pT11(H3-pT11)的去磷酸化在DNA损伤诱导的多种E2F靶向基因的转录抑制中起着至关重要的作用。在没有DNA损伤的情况下，Chk1/GCN5复合体与E2F结合，协同催化E2F启动子上的T11磷酸化和K9乙酰化，从而激活它们的转录。在DNA损伤的情况下，Chk1/GCN5复合体从E2FS中释放出来，Rb-PP1-Gamma-HDAC3复合体与E2FS结合，导致T11去磷酸化和K9去乙酰化，从而导致E2F靶向基因的转录抑制。

In this study, we found that dephosphorylation of histone H3-pT11 (H3-pT11) plays an essential role in DNA damage-induced transcriptional repression of various E2F-targeting genes. In the absence of DNA damage, Chk1/GCN5 complexes bound to E2Fs and cooperatively catalyzed T11 phosphorylation and K9 acetylation on E2F promoters, thereby activating their transcription. In the presence of DNA damage, Chk1/GCN5 complexes released from E2Fs and in place, Rb-PP1 gamma-HDAC3 complexes bound to E2Fs, leading to dephosphorylation of T11 and deacetylation of K9, which resulted in the transcriptional repression of E2F-targeting genes.