Loss of KAT6B causes premature ossification and promotes osteoblast differentiation during development
The MYST family histone acetyltransferase gene, KAT6B (MYST4, MORF, QKF) is mutated in two distinct human congenital disorders characterised by intellectual disability, facial dysmorphogenesis and skeletal abnormalities, Say-Barber-Biesecker-Young-Simpson variant of Ohdo syndrome and Genitopatellar syndrome. Despite its requirement in normal skeletal development, the cellular and transcription effects of KAT6B in skeletogenesis have not been thoroughly studied. In this dataset, we examined the effects of loss of KAT6B on gene expression in proliferating primary mouse embryonic fibroblasts (MEFs) and MEFs induced to differentiated towards chondrocytes, osteoblasts and adipocytes. We show that loss of KAT6B in mesenchymal progenitor cells promotes transition towards an osteoblast-progenitor state with upregulation of gene targets of RUNX2, a master regulators of osteoblast development and concomitant downregulation of SOX9, a critical gene in chondrocyte development. Overall design: RNA-sequencing data of mouse primary embryonic fibroblasts isolated from N = 4 Kat6b+/+ and N = 4 Kat6b–/– E12.5 mouse embryos, expanded and then grown in proliferating conditions and in conditions promoting chondrocyte, osteoblast and adipocyte differentiation.