Role of Prdm16 in fibro-adipogenic progenitors

Here, we identified Prdm16 as a FAPs-enriched factor that mediates their developmental capacities by modulating H3K9me2-marked heterochromatin organization at the nuclear lamina. We show that deletion of Prdm16 prevents FAPs adipogenic differentiation and unlocks a myogenic capacity. We found that Prdm16 localizes at the nuclear lamina where it cooperates with the H3K9 methyltransferases (KMTs), G9a and GLP, to mediate H3K9me2 deposition. RNA-seq, H3K9me2 and LaminB1 ChIP-seq, in FAPs isolated from Prdm16Flox/Flox::PdgfrαCre-ERT/+ (Prdm16) and control Prdm16Flox/Flox::Pdgfrα+/+ (WT) mice.