ArticleMechanisms of development
A dosage-dependent role for Spry2 in growth and patterning during palate development.
Article in Mechanisms of development. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.
- Genome-wide meta-analyses of nonsyndromic cleft lip with or without cleft palate identify six new risk loci.Nature genetics · 2012Pooled it
- Palatal segment contributions to midfacial anterior-posterior growth.Journal of anatomy · 2025Article
- Palatal segment contributions to midfacial anterior-posterior growth.bioRxiv : the preprint server for biology · 2024Article
- The spontaneous mouse mutant low set ears (Lse) is caused by tandem duplication of Fgf3 and Fgf4.Mammalian genome : official journal of the International Mammalian Genome Society · 2023Article
- The Evaluation ofChildren (Basel, Switzerland) · 2022Article
- Expression Analysis ofBiology · 2021Article
- Palatal rugae morphology is associated with variation in tooth number.Scientific reports · 2020Observational
- Genetics and signaling mechanisms of orofacial clefts.Birth defects research · 2020Review
- Whole genome sequencing of orofacial cleft trios from the Gabriella Miller Kids First Pediatric Research Consortium identifies a new locus on chromosome 21.Human genetics · 2020Article
- MicroRNA-124-3p suppresses mouse lip mesenchymal cell proliferation through the regulation of genes associated with cleft lip in the mouse.BMC genomics · 2019Article
- Mouse embryonic palatal mesenchymal cells maintain stemness through the PTEN-Akt-mTOR autophagic pathway.Stem cell research & therapy · 2019Article
- Haplotype and Haplotype-Environment Interaction Analysis Revealed Roles of SPRY2 for NSCL/P among Chinese Populations.International journal of environmental research and public health · 2019Article
- Wnt signaling in orofacial clefts: crosstalk, pathogenesis and models.Disease models & mechanisms · 2019Review
- A non-canonical JAGGED1 signal to JAK2 mediates osteoblast commitment in cranial neural crest cells.Cellular signalling · 2019Article
- Gene datasets associated with mouse cleft palate.Data in brief · 2018Article
- Regulation of mesenchymal signaling in palatal mucosa differentiation.Histochemistry and cell biology · 2018Article
- Lrp4/Wise regulates palatal rugae development through Turing-type reaction-diffusion mechanisms.PloS one · 2018Article
- Identification ofGenetics · 2018Article
- The Interaction of Genetic Background and Mutational Effects in Regulation of Mouse Craniofacial Shape.G3 (Bethesda, Md.) · 2017Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The formation of the palate involves the coordinated outgrowth, elevation and midline fusion of bilateral shelves leading to the separation of the oral and nasal cavities. Reciprocal signaling between adjacent fields of epithelial and mesenchymal cells directs palatal shelf growth and morphogenesis. Loss of function mutations in genes encoding FGF ligands and receptors have demonstrated a critical role for FGF signaling in mediating these epithelial-mesenchymal interactions. The Sprouty family of genes encode modulators of FGF signaling. We have established that mice carrying a deletion that removes the FGF signaling antagonist Spry2 have cleft palate. We show that excessive cell proliferation in the Spry2-deficient palate is accompanied by the abnormal progression of shape changes and movements required for medially directed shelf outgrowth and midline contact. Expression of the FGF responsive transcription factors Etv5, Msx1, and Barx1, as well as the morphogen Shh, is restricted to specific regions of the developing palate. We detected elevated and ectopic expression of these transcription factors and disorganized Shh expression in the Spry2-deficient palate. Mice carrying a targeted disruption of Spry2 fail to complement the craniofacial phenotype characterized in Spry2 deletion mice. Furthermore, a Spry2-BAC transgene rescues the palate defect. However, the BAC transgenic mouse lines express reduced levels of Spry2. The resulting hypomorphic phenotype demonstrates that palate development is Spry2 dosage sensitive. Our results demonstrate the importance of proper FGF signaling thresholds in regulation of epithelial-mesenchymal interactions and cellular responses necessary for coordinated morphogenesis of the face and palate.
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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.