Molecular and cellular mechanisms of bone catch-up growth upon cell cycle arrest

This thesis investigates how Gli1+ cartilage progenitors support bone growth under both normal and perturbed conditions. It demonstrates that Pdgfra+ perichondrial cells can transition into Gli1+ progenitors, a process regulated by Connective Tissue Growth Factor (CTGF). Using genetic mouse models with cartilage-specific cell-cycle arrest, combined with lineage tracing and transcriptomic analyses, the study shows that Gli1+ progenitors contribute to restoring growth when development is impaired. These findings improve our understanding of skeletal repair and may inform regenerative strategies targeting cartilage stem cells.