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Cullin3 promotes stem cell progeny differentiation by facilitating aPKC-directed asymmetric Numb localization

Hideyuki Komori, Noemi Rives-Quinto, Xu Han, Lucas Anhezini, Ari J. Esrig, James B. Skeath, View ORCID ProfileCheng-Yu Lee
doi: https://doi.org/10.1101/2020.07.29.227603
Hideyuki Komori
1Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA
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Noemi Rives-Quinto
1Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA
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Xu Han
1Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA
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Lucas Anhezini
1Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA
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Ari J. Esrig
1Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA
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James B. Skeath
2Department of Genetics, Washington University, Saint Louis, MO 63110, USA
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Cheng-Yu Lee
1Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA
3Division of Genetic Medicine, Department of Internal Medicine; Department of Cell and Developmental Biology; and Comprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, MI 48109 USA
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  • ORCID record for Cheng-Yu Lee
  • For correspondence: leecheng@umich.edu
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Summary

Asymmetric segregation of Numb is a conserved mechanism for regulating Notch-mediated binary cell fate decisions; however, the mechanisms controlling Numb segregation remain unclear. Previous studies have proposed an “exclusion” model, suggesting that atypical protein kinase C (aPKC) negatively regulates Numb cortical localization. Here, we report that aPKC kinase activity positively promotes basal cortical Numb localization during asymmetric division of Drosophila neural stem cells (neuroblasts) and that Cullin 3 (Cul3) is required for aPKC-directed basal Numb localization. In numb- or cul3-mutant brains, decreased levels of Numb segregated into neuroblast progeny failed to downregulate Notch, leading to supernumerary neuroblast formation. Increased aPKC kinase activity suppressed supernumerary neuroblast formation by concentrating residual Numb protein at the basal cortex and in neuroblast progeny, whereas decreased aPKC function enhanced the supernumerary neuroblast phenotype by reducing basal Numb levels. We propose that aPKC and Cul3 promote basal Numb localization, which is required to downregulate Notch signaling and promote differentiation in neuroblast progeny.

Competing Interest Statement

The authors have declared no competing interest.

Footnotes

  • ↵** Molecular, Cellular, and Integrative Biosciences Graduate Program, Pennsylvania State University

  • ↵*** Institute of Biological Sciences and Health, Universidade Federal de Alagoas, Brazil

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission.
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Posted July 29, 2020.
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Cullin3 promotes stem cell progeny differentiation by facilitating aPKC-directed asymmetric Numb localization
Hideyuki Komori, Noemi Rives-Quinto, Xu Han, Lucas Anhezini, Ari J. Esrig, James B. Skeath, Cheng-Yu Lee
bioRxiv 2020.07.29.227603; doi: https://doi.org/10.1101/2020.07.29.227603
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Cullin3 promotes stem cell progeny differentiation by facilitating aPKC-directed asymmetric Numb localization
Hideyuki Komori, Noemi Rives-Quinto, Xu Han, Lucas Anhezini, Ari J. Esrig, James B. Skeath, Cheng-Yu Lee
bioRxiv 2020.07.29.227603; doi: https://doi.org/10.1101/2020.07.29.227603

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