TWIST1 interacts with β/δ-catenins during neural tube development and regulates fate transition in cranial neural crest cells.
Cell delamination
Cell migration
Epithelial-to-mesenchymal transition
Mouse genetics
Neural tube closure
Neural tube explants
Journal
Development (Cambridge, England)
ISSN: 1477-9129
Titre abrégé: Development
Pays: England
ID NLM: 8701744
Informations de publication
Date de publication:
01 08 2022
01 08 2022
Historique:
received:
24
08
2021
accepted:
30
05
2022
pubmed:
6
7
2022
medline:
10
8
2022
entrez:
5
7
2022
Statut:
ppublish
Résumé
Cell fate determination is a necessary and tightly regulated process for producing different cell types and structures during development. Cranial neural crest cells (CNCCs) are unique to vertebrate embryos and emerge from the neural plate borders into multiple cell lineages that differentiate into bone, cartilage, neurons and glial cells. We have previously reported that Irf6 genetically interacts with Twist1 during CNCC-derived tissue formation. Here, we have investigated the mechanistic role of Twist1 and Irf6 at early stages of craniofacial development. Our data indicate that TWIST1 is expressed in endocytic vesicles at the apical surface and interacts with β/δ-catenins during neural tube closure, and Irf6 is involved in defining neural fold borders by restricting AP2α expression. Twist1 suppresses Irf6 and other epithelial genes in CNCCs during the epithelial-to-mesenchymal transition (EMT) process and cell migration. Conversely, a loss of Twist1 leads to a sustained expression of epithelial and cell adhesion markers in migratory CNCCs. Disruption of TWIST1 phosphorylation in vivo leads to epidermal blebbing, edema, neural tube defects and CNCC-derived structural abnormalities. Altogether, this study describes a previously uncharacterized function of mammalian Twist1 and Irf6 in the neural tube and CNCCs, and provides new target genes for Twist1 that are involved in cytoskeletal remodeling.
Identifiants
pubmed: 35781329
pii: 275897
doi: 10.1242/dev.200068
pmc: PMC9440756
pii:
doi:
Substances chimiques
Catenins
0
Delta Catenin
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NIDCR NIH HHS
ID : R01 DE027023
Pays : United States
Organisme : NIDCR NIH HHS
ID : U01 DE020078
Pays : United States
Organisme : NIDCR NIH HHS
ID : R01 DE016148
Pays : United States
Organisme : NIH HHS
ID : S10 OD023625
Pays : United States
Organisme : NIDCR NIH HHS
ID : R01 DE026172
Pays : United States
Informations de copyright
© 2022. Published by The Company of Biologists Ltd.
Déclaration de conflit d'intérêts
Competing interests The authors declare no competing or financial interests.
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