ArticleDevelopment (Cambridge, England)2023
FGF signaling regulates salivary gland branching morphogenesis by modulating cell adhesion.
Article in Development (Cambridge, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- High-resolution spatial transcriptomics of irradiated submandibular glands treated with fortified fibrin hydrogels.iScience · 2026Article
- Targeted regeneration of post-radiation epithelium without promoting cancer recurrence.Research square · 2026Article
- Human iPSC-derived salivary gland organoids model diabetic salivary gland dysfunction.bioRxiv : the preprint server for biology · 2025Article
- Developing and regenerating a sense of taste.Current topics in developmental biology · 2025Review
- Deletion of Fgfr2 in Ductal Basal Epithelium With Tamoxifen Induces Obstructive Meibomian Gland Dysfunction.Investigative ophthalmology & visual science · 2024Article
- Generation of salivary glands derived from pluripotent stem cells via conditional blastocyst complementation.Cell reports · 2024Article
- DiverseGenes & development · 2024Article
- DiversebioRxiv : the preprint server for biology · 2024Article
- Article
- Review
- RTK signalling promotes epithelial columnar cell shape and apical junction maintenance in human lung progenitor cells.Development (Cambridge, England) · 2023Article
- FRS2-independent GRB2 interaction with FGFR2 is not required for embryonic development.bioRxiv : the preprint server for biology · 2023Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Loss of FGF signaling leads to defects in salivary gland branching, but the mechanisms underlying this phenotype remain largely unknown. We disrupted expression of Fgfr1 and Fgfr2 in salivary gland epithelial cells and found that both receptors function coordinately in regulating branching. Strikingly, branching morphogenesis in double knockouts is restored by Fgfr1 and Fgfr2 (Fgfr1/2) knock-in alleles incapable of engaging canonical RTK signaling, suggesting that additional FGF-dependent mechanisms play a role in salivary gland branching. Fgfr1/2 conditional null mutants showed defective cell-cell and cell-matrix adhesion, both of which have been shown to play instructive roles in salivary gland branching. Loss of FGF signaling led to disordered cell-basement membrane interactions in vivo as well as in organ culture. This was partially restored upon introducing Fgfr1/2 wild-type or signaling alleles that are incapable of eliciting canonical intracellular signaling. Together, our results identify non-canonical FGF signaling mechanisms that regulate branching morphogenesis through cell-adhesion processes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.