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Mounting evidence indicates cyclin-dependent kinase (CDK) inhibitors (CKIs) of the Cip/Kip family, including p57 Kip2  and p27 Kip1 , control not only cell cycle exit but also corticogenesis. Nevertheless, distinct activities of p57 Kip2  remain poorly defined. Using in vivo and culture approaches, we show p57 Kip2  overexpression at E14.5–15.5 elicits precursor cell cycle exit, promotes transition from proliferation to neuronal differentiation, and enhances process outgrowth, while opposite effects occur in p57 Kip2 -deficient precursors. Studies at later ages indicate p57 Kip2  overexpression also induces precocious glial differentiation, suggesting stage-dependent effects. In embryonic cortex, p57 Kip2  overexpression advances cell radial migration and alters postnatal laminar positioning. While both CKIs induce differentiation, p57 Kip2  was twice as effective as p27 Kip1  in inducing neuronal differentiation and was not permissive to astrogliogenic effects of ciliary neurotrophic factor, suggesting that the CKIs differentially modulate cell fate decisions. At molecular levels, although highly conserved N-terminal regions of both CKIs elicit cycle withdrawal and differentiation, the C-terminal region of p57 Kip2  alone inhibits in vivo migration. Furthermore, p57 Kip2  effects on neurogenesis and gliogenesis require the N-terminal cyclin/CDK binding/inhibitory domains, while previous p27 Kip1  studies report cell cycle-independent functions. These observations suggest p57 Kip2  coordinates multiple stages of corticogenesis and exhibits distinct and common activities compared with related family member p27 Kip1 .

The Cyclin-Dependent Kinase Inhibitor p57 Kip2 Regulates Cell Cycle Exit, Differentiation, and Migration of Embryonic Cerebral Cortical Precursors