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

Author

Listed:
  • Susanne Laukoter

    (Institute of Science and Technology Austria)

  • Robert Beattie

    (Institute of Science and Technology Austria)

  • Florian M. Pauler

    (Institute of Science and Technology Austria)

  • Nicole Amberg

    (Institute of Science and Technology Austria)

  • Keiichi I. Nakayama

    (Kyushu University)

  • Simon Hippenmeyer

    (Institute of Science and Technology Austria)

Abstract

The cyclin-dependent kinase inhibitor p57KIP2 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.

Suggested Citation

  • Susanne Laukoter & Robert Beattie & Florian M. Pauler & Nicole Amberg & Keiichi I. Nakayama & Simon Hippenmeyer, 2020. "Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development," Nature Communications, Nature, vol. 11(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-019-14077-2
    DOI: 10.1038/s41467-019-14077-2
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