A desmosomal cadherin controls multipotent hair follicle stem cell quiescence and orchestrates regeneration through adhesion signaling.
Cell biology
Molecular biology
Journal
iScience
ISSN: 2589-0042
Titre abrégé: iScience
Pays: United States
ID NLM: 101724038
Informations de publication
Date de publication:
15 Dec 2023
15 Dec 2023
Historique:
received:
06
09
2023
revised:
03
11
2023
accepted:
21
11
2023
medline:
2
1
2024
pubmed:
2
1
2024
entrez:
1
1
2024
Statut:
epublish
Résumé
Stem cells (SCs) are critical to maintain tissue homeostasis. However, it is currently not known whether signaling through cell junctions protects quiescent epithelial SC reservoirs from depletion during disease-inflicted damage. Using the autoimmune model disease pemphigus vulgaris (PV), this study reveals an unprecedented role for a desmosomal cadherin in governing SC quiescence and regeneration through adhesion signaling in the multipotent mouse hair follicle compartment known as the bulge. Autoantibody-mediated, mechanical uncoupling of desmoglein (Dsg) 3 transadhesion activates quiescent bulge SC which lose their multipotency and stemness, become actively cycling, and finally delaminate from their epithelial niche. This then initiates a self-organized regenerative program which restores Dsg3 function and bulge morphology including SC quiescence and multipotency. These profound changes are triggered by the sole loss of functional Dsg3, resemble major signaling events in
Identifiants
pubmed: 38162019
doi: 10.1016/j.isci.2023.108568
pii: S2589-0042(23)02645-7
pmc: PMC10755723
doi:
Types de publication
Journal Article
Langues
eng
Pagination
108568Informations de copyright
© 2023 The Author(s).
Déclaration de conflit d'intérêts
The last author (E.J.M.) is a founder and director of the board of CELLnTEC Advanced Cell Systems AG. We used CELLnTEC media in this study. All other authors have declared no conflict of interest.