ChIP-seq analysis of H3K27ac in K562 cells with shRNA-mediated depeltion of TFAM expression

The developing erythroid cells require highly coordinated gene expression and metabolism. By comparing the proteomic and transcriptomic changes in human hematopoietic stem/progenitor cells (HSPCs) and lineage-committed erythroid progenitors (ProEs), and uncover pathways related to mitochondrial biogenesis enhanced through post-transcriptional regulation. Two principal mitochondrial factors TFAM and PHB2 are tightly regulated at the protein level and indispensable for mitochondria and erythropoiesis. Depletion of TFAM in erythroid cells alters intracellular metabolism, leading to elevated histone acetylation, deregulated gene expression, defective mitochondria function and erythropoiesis. To examine the global effects of histone hyperactylation in Tfam-deficient erythroid cells, we performed ChIP-seq analysis of H3K27ac in human K562 cells transduced with TFAM-specific or control (shNT) shRNAs.