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FAM83H couples keratin organization to Notch signaling during epidermal morphogenesis
Biorxiv : the Preprint Server for Biology
|June 29, 2026
Summary
FAM83H is a newly discovered regulator that connects keratin structure to cell fate in the epidermis. Its loss impairs keratinocyte differentiation and epidermal development by disrupting cell junctions and Notch signaling.
Area of Science:
- Cell Biology
- Developmental Biology
- Dermatology
Background:
- Keratin intermediate filaments are crucial for skin integrity.
- The link between keratin organization and keratinocyte cell fate signaling during epidermal development is unclear.
Purpose of the Study:
- To identify novel regulators connecting keratin organization with epidermal cell fate.
- To elucidate the mechanism by which FAM83H influences epidermal morphogenesis and keratinocyte differentiation.
Main Methods:
- Utilized mouse models and a human 3D microphysiological epidermis model.
- Performed single-cell transcriptomic analysis to identify signaling pathways affected by FAM83H loss.
- Investigated the molecular localization and function of FAM83H at cell-cell junctions.
Main Results:
- FAM83H loss disrupts epidermal architecture, impairs basal keratinocyte differentiation, organization, and cell-cell adhesion.
- FAM83H depletion is associated with alterations in Notch signaling pathways.
- FAM83H organizes keratin filaments and desmosome integrity at cell junctions, impacting a desmoplakin-keratin-Notch1 complex and Notch1 activation.
Conclusions:
- FAM83H is a key regulator of epidermal morphogenesis, coupling keratin cytoskeletal architecture to Notch1 signaling.
- Keratin-associated proteins, like FAM83H, actively participate in epithelial fate decisions governing epidermal homeostasis.
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