ArticleDevelopmental biology2007
phospholipase C, beta 3 is required for Endothelin1 regulation of pharyngeal arch patterning in zebrafish.
Article in Developmental biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 68 citations in OpenAlex.
- The Gq/11 family of Gα subunits is necessary and sufficient for lower jaw development.Development (Cambridge, England) · 2025Article
- Endothelin signaling in development.Development (Cambridge, England) · 2023Review
- Knockdown of hspg2 is associated with abnormal mandibular joint formation and neural crest cell dysfunction in zebrafish.BMC developmental biology · 2021Article
- Selective breeding modifies mef2ca mutant incomplete penetrance by tuning the opposing Notch pathway.PLoS genetics · 2019Article
- Genome-wide analysis of facial skeletal regionalization in zebrafish.Development (Cambridge, England) · 2017Article
- Nkx2.5 regulates endothelin converting enzyme-1 during pharyngeal arch patterning.Genesis (New York, N.Y. : 2000) · 2017Article
- Building and maintaining joints by exquisite local control of cell fate.Wiley interdisciplinary reviews. Developmental biology · 2017Review
- The old and new face of craniofacial research: How animal models inform human craniofacial genetic and clinical data.Developmental biology · 2016Review
- Competition between Jagged-Notch and Endothelin1 Signaling Selectively Restricts Cartilage Formation in the Zebrafish Upper Face.PLoS genetics · 2016Article
- Genomics of Rapid Incipient Speciation in Sympatric Threespine Stickleback.PLoS genetics · 2016Article
- Cre recombinase-regulated Endothelin1 transgenic mouse lines: novel tools for analysis of embryonic and adult disorders.Developmental biology · 2015Article
- Zebrafish Craniofacial Development: A Window into Early Patterning.Current topics in developmental biology · 2015Review
- Mutations in endothelin 1 cause recessive auriculocondylar syndrome and dominant isolated question-mark ears.American journal of human genetics · 2013Article
- Understanding the basis of auriculocondylar syndrome: Insights from human, mouse and zebrafish genetic studies.American journal of medical genetics. Part C, Seminars in medical genetics · 2013Review
- barx1 represses joints and promotes cartilage in the craniofacial skeleton.Development (Cambridge, England) · 2013Article
- Phosphoinositides: tiny lipids with giant impact on cell regulation.Physiological reviews · 2013Review
- Article
- New perspectives on pharyngeal dorsoventral patterning in development and evolution of the vertebrate jaw.Developmental biology · 2012Review
- Revealing the role of phospholipase Cβ3 in the regulation of VEGF-induced vascular permeability.Blood · 2012Article
- Hh signaling regulates patterning and morphogenesis of the pharyngeal arch-derived skeleton.Developmental biology · 2012Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Genetic and pharmacological studies demonstrate that Endothelin1 (Edn1) is a key signaling molecule for patterning the facial skeleton in fish, chicks, and mice. When Edn1 function is reduced early in development the ventral lower jaw and supporting structures are reduced in size and often fused to their dorsal upper jaw counterparts. We show that schmerle (she) encodes a zebrafish ortholog of Phospholipase C, beta 3 (Plcbeta3) required in cranial neural crest cells for Edn1 regulation of pharyngeal arch patterning. Sequencing and co-segregation demonstrates that two independent she (plcbeta3) alleles have missense mutations in conserved residues within the catalytic domains of Plcbeta3. Homozygous plcbeta3 mutants are phenotypically similar to edn1 mutants and exhibit a strong arch expression defect in Edn1-dependent Distalless (Dlx) genes as well as expression defects in several Edn1-dependent intermediate and ventral arch domain transcription factors. plcbeta3 also genetically interacts with edn1, supporting a model in which Edn1 signals through a G protein-coupled receptor to activate Plcbeta3. Mild skeletal defects occur in plcbeta3 heterozygotes, showing the plcbeta3 mutations are partially dominant. Through a morpholino-mediated deletion in the N-terminal PH domain of Plcbeta3, we observe a partial rescue of facial skeletal defects in homozygous plcbeta3 mutants, supporting a hypothesis that an intact PH domain is necessary for the partial dominance we observe. In addition, through mosaic analyses, we show that wild-type neural crest cells can efficiently rescue facial skeletal defects in homozygous plcbeta3 mutants, demonstrating that Plcbeta3 function is required in neural crest cells and not other cell types to pattern the facial skeleton.
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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.