Various types of neurons and glia are generated following a precise spatial and temporal order during neurogenesis. The mechanisms that control this sequential generation of neuronal and glial cell types from the same progenitor population are not well understood. Growth differentiation factor 11 (Gdf11) belongs to the TGF-β family of proteins and is expressed transiently in newly born neurons adjacent to the progenitor domain in the developing spinal cord. We examined the phenotypes ofGdf11−/−mouse embryos and found that without Gdf11, neuronal differentiation in the spinal cord progresses at a slower rate. Higher progenitor proliferation rate, along with a delay in gliogenesis, is also observed inGdf11−/−spinal cord but only after the peak ofGdf11expression, indicating that Gdf11 can cause long-lasting changes in progenitor properties. These changes can be preservedin vitro, as neurospheres derived fromGdf11−/−and wild-type littermates at a stage after, but not before the onset ofGdf11expression, exhibit differences in proliferation and differentiation potential. Moreover, these changes in progenitor properties can be inducedin vitroby the addition of Gdf11. We also demonstrate that the effects of Gdf11 on progenitor cells are associated with its ability to upregulate p57Kip2and p27Kip1while downregulating Pax6 expression. These results support a model in which Gdf11 secreted by newly born neurons in the developing spinal cord facilitates the temporal progression of neurogenesis by acting as a positive feedback signal on the progenitor cells to promote cell cycle exit and decrease proliferation ability, thus changing their differentiation potential.