Sox11 And Sox4 Drive The Reactivation Of An Embryonic Gene Program During Murine Wound Repair

The study demonstrated that during wound repair in a mouse model, epidermal cells at the wound edge reverted to an embryonic-like state, significantly altering cytoskeletal and extracellular matrix components. SOX11 and SOX4 were identified as key regulators of this process, controlling genes related to epidermal development and cytoskeletal organization. Inducing SOX11 postnatally repressed epidermal differentiation, while deficiencies in SOX11 and SOX4 accelerated differentiation and impaired cell motility and re-epithelialization. The study highlighted fascin actin-bundling protein 1 (FSCN1) as a crucial target of SOX11 and SOX4, essential for cell migration, thus underscoring the importance of these factors in reactivating an embryonic gene program during wound repair.