ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2014
Endoderm-specific deletion of Tbx1 reveals an FGF-independent role for Tbx1 in pharyngeal apparatus morphogenesis.
Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- Paxillin is crucial for thymus and parathyroid development by regulating the architecture of the third pharyngeal pouch endoderm.Cellular and molecular life sciences : CMLS · 2026Article
- Tbx1 haploinsufficiency leads to local skull deformity, paraflocculus and flocculus dysplasia, and motor-learning deficit in 22q11.2 deletion syndrome.Nature communications · 2024Article
- Transcriptional and epigenetic characterization of a new in vitro platform to model the formation of human pharyngeal endoderm.Genome biology · 2024Article
- A Potential Role ofDevelopment & reproduction · 2024Article
- Molecular Pathways and Animal Models of Semilunar Valve and Aortic Arch Anomalies.Advances in experimental medicine and biology · 2024Review
- Single-cell transcriptomics uncovers a non-autonomous Tbx1-dependent genetic program controlling cardiac neural crest cell development.Nature communications · 2023Article
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- Inactivation of Fgf3 and Fgf4 within the Fgf3/Fgf4/Fgf15 gene cluster reveals their redundant requirement for mouse inner ear induction and embryonic survival.Developmental dynamics : an official publication of the American Association of Anatomists · 2022Article
- Morphogenesis of the Mammalian Aortic Arch Arteries.Frontiers in cell and developmental biology · 2022Article
- The Mandibular and Hyoid Arches-From Molecular Patterning to Shaping Bone and Cartilage.International journal of molecular sciences · 2021Review
- Thymus Inception: Molecular Network in the Early Stages of Thymus Organogenesis.International journal of molecular sciences · 2020Review
- Article
- TBX1 is required for normal stria vascularis and semicircular canal development.Developmental biology · 2020Article
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- Tbx1 and Foxi3 genetically interact in the pharyngeal pouch endoderm in a mouse model for 22q11.2 deletion syndrome.PLoS genetics · 2019Article
- Cellular organization and boundary formation in craniofacial development.Genesis (New York, N.Y. : 2000) · 2019Review
- Asymmetry in Mechanosensitive Gene Expression during Aortic Arch Morphogenesis.Scientific reports · 2018Article
- Molecular genetics of 22q11.2 deletion syndrome.American journal of medical genetics. Part A · 2018Review
- Dysregulation of TBX1 dosage in the anterior heart field results in congenital heart disease resembling the 22q11.2 duplication syndrome.Human molecular genetics · 2018Article
- An FGF3-BMP Signaling Axis Regulates Caudal Neural Tube Closure, Neural Crest Specification and Anterior-Posterior Axis Extension.PLoS genetics · 2016Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThe T-box transcription factor Tbx1, is essential for the normal development of multiple organ systems in the embryo. One of the most striking phenotypes in Tbx1-/- embryos is the failure of the caudal pharyngeal pouches to evaginate from the foregut endoderm. Despite considerable interest in the role of Tbx1 in development, the mechanisms whereby Tbx1 controls caudal pouch formation have remained elusive. In particular, the question as to how Tbx1 expression in the pharyngeal endoderm regulates pharyngeal pouch morphogenesis in the mouse embryo is not known.
resultsTo address this question, we produced mouse embryos in which Tbx1 was specifically deleted from the pharyngeal endoderm and, as expected, embryos failed to form caudal pharyngeal pouches. To determine the molecular mechanism, we examined expression of Fgf3 and Fgf8 ligands and downstream effectors. Although Fgf8 expression is greatly reduced in Tbx1-deficient endoderm, FGF signaling levels are unaffected. Furthermore, pouch morphogenesis is only partially perturbed by the loss of both Fgf3 and Fgf8 from the endoderm, indicating that neither are required for pouch formation.
conclusionsTbx1 deletion from the pharyngeal endoderm is sufficient to cause caudal pharyngeal arch segmentation defects by FGF-independent effectors that remain to be identified.
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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.