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Notch1 cortical signaling regulates epithelial architecture and cell-cell adhesion

Matthew J. White, View ORCID ProfileKyle A. Jacobs, View ORCID ProfileTania Singh, View ORCID ProfileMatthew L. Kutys
doi: https://doi.org/10.1101/2023.01.23.524428
Matthew J. White
1Department of Cell and Tissue Biology, University of California San Francisco, San Francisco CA, 94143, USA
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Kyle A. Jacobs
1Department of Cell and Tissue Biology, University of California San Francisco, San Francisco CA, 94143, USA
2Biomedical Sciences Graduate Program, University of California San Francisco, San Francisco CA, 94143, USA
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Tania Singh
1Department of Cell and Tissue Biology, University of California San Francisco, San Francisco CA, 94143, USA
3Joint Graduate Program in Bioengineering, University of California San Francisco, University of California Berkeley, San Francisco CA, 94143, USA
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Matthew L. Kutys
1Department of Cell and Tissue Biology, University of California San Francisco, San Francisco CA, 94143, USA
2Biomedical Sciences Graduate Program, University of California San Francisco, San Francisco CA, 94143, USA
3Joint Graduate Program in Bioengineering, University of California San Francisco, University of California Berkeley, San Francisco CA, 94143, USA
4Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco CA, 94143, USA
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  • For correspondence: matthew.kutys@ucsf.edu
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SUMMARY

Notch receptors control tissue morphogenic processes that involve coordinated changes in cell architecture and gene expression, but how a single receptor can produce these diverse biological outputs is unclear. Here we employ a 3D organotypic model of a ductal epithelium to reveal tissue morphogenic defects result from loss of Notch1, but not Notch1 transcriptional signaling. Instead, defects in duct morphogenesis are driven by dysregulated epithelial cell architecture and mitogenic signaling which result from loss of a transcription-independent Notch1 cortical signaling mechanism that ultimately functions to stabilize adherens junctions and cortical actin. We identify that Notch1 localization and cortical signaling are tied to apical-basal cell restructuring and discover a Notch1-FAM83H interaction underlies stabilization of adherens junctions and cortical actin. Together, these results offer new insights into Notch1 signaling and regulation, and advance a paradigm in which transcriptional and cell adhesive programs might be coordinated by a single receptor.

Competing Interest Statement

The authors have declared no competing interest.

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC 4.0 International license.
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Posted January 23, 2023.
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Notch1 cortical signaling regulates epithelial architecture and cell-cell adhesion
Matthew J. White, Kyle A. Jacobs, Tania Singh, Matthew L. Kutys
bioRxiv 2023.01.23.524428; doi: https://doi.org/10.1101/2023.01.23.524428
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Notch1 cortical signaling regulates epithelial architecture and cell-cell adhesion
Matthew J. White, Kyle A. Jacobs, Tania Singh, Matthew L. Kutys
bioRxiv 2023.01.23.524428; doi: https://doi.org/10.1101/2023.01.23.524428

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