An understanding of the diversity of neural progenitors and flexibility in their fate choices - lineage plasticity - is crucial for understanding how complex organs like the brain are generated or undergo repair. The neonatal mouse cerebellum is a powerful model to uncover regenerative responses. We have shown that the cerebellum can recover from injury at birth via distinct mechanisms. In one case, when granule cell progenitors are ablated, a subpopulation of the nestin-expressing progenitors (NEPs) that normally generate glia undergoes adaptive reprogramming and replenishes some of the lost granule cell progenitors. Interestingly, the regenerative potential of the neonatal cerebellum dramatically decreases once development ends, despite the presence of NEP-like cells in the adult cerebellum. Our lab is interested in two questions: 1)What are the mechanisms that enable regeneration in the neonates and inhibit in the adult cerebellum? 2)Can we facilitate regeneration in the brain?