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The cyclin-dependent kinase inhibitor p57 KIP2  is encoded by the imprinted  Cdkn1c  locus, exhibits maternal expression, and is essential for cerebral cortex development. How  Cdkn1c  regulates corticogenesis is however not clear. To this end we employ Mosaic Analysis with Double Markers (MADM) technology to genetically dissect  Cdkn1c  gene function in corticogenesis at single cell resolution. We find that the previously described growth-inhibitory  Cdkn1c  function is a non-cell-autonomous one, acting on the whole organism. In contrast we reveal a growth-promoting cell-autonomous  Cdkn1c  function which at the mechanistic level mediates radial glial progenitor cell and nascent projection neuron survival. Strikingly, the growth-promoting function of  Cdkn1c  is highly dosage sensitive but not subject to genomic imprinting. Collectively, our results suggest that the  Cdkn1c  locus regulates cortical development through distinct cell-autonomous and non-cell-autonomous mechanisms. More generally, our study highlights the importance to probe the relative contributions of cell intrinsic gene function and tissue-wide mechanisms to the overall phenotype.

Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development