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损伤诱导的各种e2f靶向基因的转录抑制中起重要作用。在没有DNA损伤的情况下，Chk1/GCN5复合物结合到E2F上，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。在存在DNA损伤的情况下，Chk1/GCN5复合物从E2Fs中释放出来，Rb-PP1 γ - hdac3复合物与E2Fs结合，导致T11的去磷酸化和K9的去乙酰化，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.