Genome-wide H3K56ac profiling after Sirt6 knockdown in mESCs [ChIP-seq]

Sirt6, the NAD+-dependent deacetylase, has been described to deacetylate H3K9, H3K18, and H3K56. However, analysis of the acetylation status revealed that loss of Sirt6 caused a massive increase of histone H3K56ac levels but no detectable change of histone H3K9ac and H3K18ac, indicating that SIRT6 is the dominant deacetylase for H3K56ac in muscle stem cells (MuSCs). Further, we investigate genome-wide H3K56ac profiling in the absence of Sirt6 in MuSCs and mouse embryonic stem cells (mESCs) using high throughput sequencing (ChIP-seq). ChIP-seq experiment to determine genome-wide H3K56ac distribution in scrabled control and Sirt6 knockdown mouse embryonic stem cells

Sirt6作为NAD+依赖型脱乙酰基酶（NAD+-dependent deacetylase），已被报道可介导组蛋白H3K9、H3K18及H3K56的脱乙酰化修饰。然而，乙酰化状态分析结果显示，Sirt6缺失会导致组蛋白H3K56乙酰化（H3K56ac）水平显著升高，但组蛋白H3K9乙酰化（H3K9ac）与H3K18乙酰化（H3K18ac）水平未出现可检测到的变化，这表明在肌肉干细胞（Muscle Stem Cells, MuSCs）中，SIRT6是调控H3K56ac的核心脱乙酰基酶。进一步地，本研究采用高通量测序技术（ChIP-seq，Chromatin Immunoprecipitation Sequencing，染色质免疫共沉淀测序），对肌肉干细胞与小鼠胚胎干细胞（mouse embryonic stem cells, mESCs）中Sirt6缺失后的全基因组H3K56ac分布特征展开分析。此外，本研究还针对阴性对照（scrambled control）与Sirt6敲低的小鼠胚胎干细胞，开展了全基因组H3K56ac分布检测的ChIP-seq实验。