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During mammalian brain development, radial glial progenitors balance between proliferation and differentiation to generate the laminated cortical layers in a temporally precise fashion. Defects in the individual steps going into this complex organogenesis can result in cortical malformations and human nervous system disorders. In this issue of  Genes &amp; Development , Liu and colleagues (pp. 763–780) present experimental evidence that an evolutionarily conserved cellular polarity gene,  Pard3  ( partitioning-defective 3 ), controls the balance of radial glial proliferation and differentiation through interaction with the Hippo signal transduction pathway. Conditional deletion of  Pard3  in the developing rodent cortex resulted in striking subcortical band heterotopia, reminiscent of a severe form of human cortical malformation.

Laminating the mammalian cortex during development: cell polarity protein function and Hippo signaling