ArticleDevelopmental biology2014
Multiple tissue-specific requirements for the BMP antagonist Noggin in development of the mammalian craniofacial skeleton.
Article in Developmental biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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
18 citing papers in PubMed, 29 citations in OpenAlex.
- Genetic architecture of craniofacial morphogenesis: roles ofFrontiers in cell and developmental biology · 2026Review
- Haploinsufficiency of GRHL2 is associated with orofacial clefting in humans.Human molecular genetics · 2025Article
- Cranial base synostosis in mice caused by upregulation of Wnt following partial inhibition of Shh.BMC biology · 2025Article
- Grainyhead-like 2 interacts with noggin to regulate tissue fusion in mouse.Development (Cambridge, England) · 2024Article
- Taste papilla cell differentiation requires the regulation of secretory protein production by ALK3-BMP signaling in the tongue mesenchyme.Development (Cambridge, England) · 2023Article
- Evolutionary mechanisms modulating the mammalian skull development.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- GRHL2 and AP2a coordinate early surface ectoderm lineage commitment during development.iScience · 2023Article
- Complex genetic architecture of three-dimensional craniofacial shape variation in domestic pigeons.Evolution & development · 2021Article
- Why Does the Face Predict the Brain? Neural Crest Induction, Craniofacial Morphogenesis, and Neural Circuit Development.Frontiers in physiology · 2020Review
- The balance of Bmp6 and Wnt10b regulates the telogen-anagen transition of hair follicles.Cell communication and signaling : CCS · 2019Article
- Wnt signaling in orofacial clefts: crosstalk, pathogenesis and models.Disease models & mechanisms · 2019Review
- Regulatory mechanisms of jaw bone and tooth development.Current topics in developmental biology · 2019Review
- PLGA-based control release of Noggin blocks the premature fusion of cranial sutures caused by retinoic acid.Applied microbiology and biotechnology · 2019Article
- Gene datasets associated with mouse cleft palate.Data in brief · 2018Article
- Non-syndromic Cleft Lip and Palate Polymorphisms Affect Normal Lip Morphology.Frontiers in genetics · 2018Article
- BMPR1B mutation causes Pierre Robin sequence.Oncotarget · 2017Article
- ISLET1-Dependent β-Catenin/Hedgehog Signaling Is Required for Outgrowth of the Lower Jaw.Molecular and cellular biology · 2017Article
- Common mechanisms in development and disease: BMP signaling in craniofacial development.Cytokine & growth factor reviews · 2016Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Proper morphogenesis is essential for both form and function of the mammalian craniofacial skeleton, which consists of more than twenty small cartilages and bones. Skeletal elements that support the oral cavity are derived from cranial neural crest cells (NCCs) that develop in the maxillary and mandibular buds of pharyngeal arch 1 (PA1). Bone Morphogenetic Protein (BMP) signaling has been implicated in most aspects of craniofacial skeletogenesis, including PA1 development. However, the roles of the BMP antagonist Noggin in formation of the craniofacial skeleton remain unclear, in part because of its multiple domains of expression during formative stages. Here we used a tissue-specific gene ablation approach to assess roles of Noggin (Nog) in two different tissue domains potentially relevant to mandibular and maxillary development. We found that the axial midline domain of Nog expression is critical to promote PA1 development in early stages, necessary for adequate outgrowth of the mandibular bud. Subsequently, Nog expression in NCCs regulates craniofacial cartilage and bone formation. Mice lacking Nog in NCCs have an enlarged mandible that results from increased cell proliferation in and around Meckel׳s cartilage. These mutants also show complete secondary cleft palate, most likely due to inhibition of posterior palatal shelf elevation by disrupted morphology of the developing skull base. Our findings demonstrate multiple roles of Noggin in different domains for craniofacial skeletogenesis, and suggest an indirect mechanism for secondary cleft palate in Nog mutants that may be relevant to human cleft palate as well.
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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.