ArticleDevelopmental biology2011
Pax3 is essential for normal cardiac neural crest morphogenesis but is not required during migration nor outflow tract septation.
Article in Developmental biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 61 citations in OpenAlex.
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- Evaluating possible maternal effect lethality and genetic background effects inbioRxiv : the preprint server for biology · 2024Article
- SMAD4: A critical regulator of cardiac neural crest cell fate and vascular smooth muscle development.Developmental dynamics : an official publication of the American Association of Anatomists · 2024Article
- Evaluating possible maternal effect lethality and genetic background effects in Naa10 knockout mice.PloS one · 2024Article
- Molecular Pathways and Animal Models of Truncus Arteriosus.Advances in experimental medicine and biology · 2024Review
- KCTD1/KCTD15 complexes control ectodermal and neural crest cell functions, and their impairment causes aplasia cutis.The Journal of clinical investigation · 2023Article
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- PAX Genes in Cardiovascular Development.International journal of molecular sciences · 2022Review
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- Pitx2 Differentially Regulates the Distinct Phases of Myogenic Program and Delineates Satellite Cell Lineages During Muscle Development.Frontiers in cell and developmental biology · 2022Article
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- Altered sacral neural crest development in Pax3 spina bifida mutants underlies deficits of bladder innervation and function.Developmental biology · 2021Article
- Cardiac Neural Crest Cells: Their Rhombomeric Specification, Migration, and Association with Heart and Great Vessel Anomalies.Cellular and molecular neurobiology · 2021Review
- Sox10-cre BAC transgenes reveal temporal restriction of mesenchymal cranial neural crest and identify glandular Sox10 expression.Developmental biology · 2021Article
- Early Embryonic Expression ofJournal of cardiovascular development and disease · 2020Article
- Why Does the Face Predict the Brain? Neural Crest Induction, Craniofacial Morphogenesis, and Neural Circuit Development.Frontiers in physiology · 2020Review
- Armadillo-like helical domain containing-4 is dynamically expressed in both the first and second heart fields.Gene expression patterns : GEP · 2019Article
- Loss of CXCL12/CXCR4 signalling impacts several aspects of cardiovascular development but does not exacerbate Tbx1 haploinsufficiency.PloS one · 2018Article
- Pdgfrα functions in endothelial-derived cells to regulate neural crest cells and the development of the great arteries.Disease models & mechanisms · 2017Article
- Temporally Distinct Six2-Positive Second Heart Field Progenitors Regulate Mammalian Heart Development and Disease.Cell reports · 2017Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Systemic loss-of-function studies have demonstrated that Pax3 transcription factor expression is essential for dorsal neural tube, early neural crest and muscle cell lineage morphogenesis. Cardiac neural crest cells participate in both remodeling of the pharyngeal arch arteries and outflow tract septation during heart development, but the lineage specific role of Pax3 in neural crest function has not yet been determined. To gain insight into the requirement of Pax3 within the neural crest, we conditionally deleted Pax3 in both the premigratory and migratory neural crest populations via Wnt1-Cre and Ap2α-Cre and via P0-Cre in only the migratory neural crest, and compared these phenotypes to the pulmonary atresia phenotype observed following the systemic loss of Pax3. Surprisingly, using Wnt1-Cre deletion there are no resultant heart defects despite the loss of Pax3 from the premigratory and migratory neural crest. In contrast, earlier premigratory and migratory Ap2α-Cre mediated deletion resulted in double outlet right ventricle alignment heart defects. In order to assess the tissue-specific contribution of neural crest to heart development, genetic ablation of neural crest lineage using a Wnt1-Cre-activated diphtheria toxin fragment-A cell-killing system was employed. Significantly, ablation of Wnt1-Cre-expressing neural crest cells resulted in fully penetrant persistent truncus arteriosus malformations. Combined, the data show that Pax3 is essential for early neural crest progenitor formation, but is not required for subsequent cardiac neural crest progeny morphogenesis involving their migration to the heart or septation of the outflow tract.
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