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Loss of coiled-coil protein Cep55 impairs abscission processes and results in p53-dependent apoptosis in developing cortex

View ORCID ProfileJessica N. Little, View ORCID ProfileKatrina C. McNeely, View ORCID ProfileNadine Michel, View ORCID ProfileChristopher J. Bott, View ORCID ProfileKaela S. Lettieri, Madison R. Hecht, Sara A. Martin, View ORCID ProfileNoelle D. Dwyer
doi: https://doi.org/10.1101/2020.06.02.129346
Jessica N. Little
1Department of Cell Biology, University of Virginia School of Medicine, Charlottesville, VA, USA
3Medical Scientist Training Program, University of Virginia School of Medicine, Charlottesville, VA, USA
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Katrina C. McNeely
1Department of Cell Biology, University of Virginia School of Medicine, Charlottesville, VA, USA
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Nadine Michel
2Department of Biochemistry and Molecular Genetics, University of Virginia School of Medicine, Charlottesville, VA, USA
3Medical Scientist Training Program, University of Virginia School of Medicine, Charlottesville, VA, USA
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Christopher J. Bott
1Department of Cell Biology, University of Virginia School of Medicine, Charlottesville, VA, USA
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Kaela S. Lettieri
1Department of Cell Biology, University of Virginia School of Medicine, Charlottesville, VA, USA
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Madison R. Hecht
1Department of Cell Biology, University of Virginia School of Medicine, Charlottesville, VA, USA
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Sara A. Martin
1Department of Cell Biology, University of Virginia School of Medicine, Charlottesville, VA, USA
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Noelle D. Dwyer
1Department of Cell Biology, University of Virginia School of Medicine, Charlottesville, VA, USA
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  • For correspondence: ndwyer@virginia.edu
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Abstract

To produce a brain of normal size and structure, embryonic neural stem cell (NSCs) must tightly regulate their cell divisions. Cerebral cortex NSCs undergo a polarized form of cytokinesis whose regulation is poorly understood. Cytokinetic abscission severs the daughter cells and is mediated by the midbody at the apical membrane. Here we elucidate the role of the coiled-coil midbody protein Cep55 in NSC abscission and brain development. A knockout of Cep55 in mice causes microcephaly with reduced NSCs and neurons, but relatively normal body size. Fixed and live analyses show NSCs lacking Cep55 have decreased but not eliminated ESCRT recruitment, and have abnormal abscission and higher rates of failure. P53-mediated apoptosis is greatly increased in the brain, but not other tissues, and p53 knockout partly rescues brain size. Thus, loss of Cep55 causes abscission defects and failures in multiple cell types, but the secondary p53 response and apoptosis is brain-specific.

Competing Interest Statement

The authors have declared no competing interest.

Footnotes

  • ↵* co-first author

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Posted June 03, 2020.
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Loss of coiled-coil protein Cep55 impairs abscission processes and results in p53-dependent apoptosis in developing cortex
Jessica N. Little, Katrina C. McNeely, Nadine Michel, Christopher J. Bott, Kaela S. Lettieri, Madison R. Hecht, Sara A. Martin, Noelle D. Dwyer
bioRxiv 2020.06.02.129346; doi: https://doi.org/10.1101/2020.06.02.129346
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Loss of coiled-coil protein Cep55 impairs abscission processes and results in p53-dependent apoptosis in developing cortex
Jessica N. Little, Katrina C. McNeely, Nadine Michel, Christopher J. Bott, Kaela S. Lettieri, Madison R. Hecht, Sara A. Martin, Noelle D. Dwyer
bioRxiv 2020.06.02.129346; doi: https://doi.org/10.1101/2020.06.02.129346

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