Bap1 promotes osteoclast function by metabolic reprogramming
The deubiquitinase activity of Bap1 modifies osteoclast function by metabolic reprogramming. Bap1 deficient osteoclast lineage cells upregulate the cystine transporter, Slc7a11, by enhanced H2Aub occupancy of its promoter. SLC7A11 controls cellular ROS levels and redirects the mitochondrial metabolites away from the TCA cycle, both of which are necessary for osteoclast function. Overall design: Bone marrow macrophages from Bap1flox and Bap1LysM mice were treated with MCSF and RANKL for 24 hrs. RNA was extracted for RNAseq study