Mutant p53 alters chromatin accessibility in hematopoietic stem and progenitor cells [ATAC-seq]

To investigate how mutant p53 regulates gene transcription in HSPCs, we performed ATAC-seq assays in LSKs to identify differential regions of chromatin accessibility. We obsreved approximately 600 peaks significantly increased chromatin accessibility in mutant p53 LSKs compared to wild type p53 LSKs. Overall design: To elucidate the mechanism of how mutant p53 regulates gene transcription in hematopoietic stem an dprogenitor cells (HSPCs), we sorted Lin-Sca1+Kit+ cells LSKs) from the bone marrow of p53+/+ and p53R248W/+ mice and then perfromed ATAC-seq assays.

为探究突变型p53如何在造血干细胞和祖细胞（hematopoietic stem and progenitor cells, HSPCs）中调控基因转录，我们在LSK细胞中开展了ATAC-seq实验以鉴定染色质可及性差异区域。我们观察到，相较于野生型p53 LSK细胞，突变型p53 LSK细胞中约有600个染色质可及性显著升高的峰。实验整体设计：为阐明突变型p53调控造血干细胞和祖细胞（HSPCs）基因转录的机制，我们从p53+/+及p53R248W/+小鼠的骨髓中分选得到Lin-Sca1+Kit+细胞（即LSK细胞），随后进行了ATAC-seq实验。