ArticleGastroenterology2022
Direct Interaction of Sox10 With Cadherin-19 Mediates Early Sacral Neural Crest Cell Migration: Implications for Enteric Nervous System Development Defects.
Article in Gastroenterology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Targeting the nervous system: Mechanistic insights into neuro-tumor communication and therapeutic opportunities.Acta pharmaceutica Sinica. B · 2026Review
- Cadherin 19 deficiency inhibits osteogenic differentiation and bone formation by regulating PI3K/AKT signaling pathway.Stem cell research & therapy · 2026Article
- A Novel Anti-Cadherin-19 Monoclonal Antibody (CaCurrent issues in molecular biology · 2026Article
- Enamel decussation pattern originates from directional sliding of ameloblasts.International journal of oral science · 2026Article
- Tracing the enteric neural crest cell pathway from origin to colonization: insights into Hirschsprung's disease.Molecular biology reports · 2025Review
- hPSC-derived sacral neural crest cells restore erectile function in pelvic ganglia injury.Stem cell research & therapy · 2025Article
- Intramuscular enteric glia persist in Hirschsprung disease and undergo neurogenesis in response to GDNF-NCAM1 signaling.Scientific reports · 2025Article
- EMB is essential for enteric nervous system development mediated by PI3K signaling.Genome medicine · 2025Article
- A framework for target discovery in rare cancers.bioRxiv : the preprint server for biology · 2024Article
- Molecular heterogeneity of quiescent melanocyte stem cells revealed by single-cell RNA-sequencing.Pigment cell & melanoma research · 2024Article
- Aberrant SOX10 and RET expressions in patients with Hirschsprung disease.BMC pediatrics · 2024Article
- Article
- Hirschsprung disease.Nature reviews. Disease primers · 2023Review
- GWAS using low-pass whole genome sequence reveals a novel locus in canine congenital idiopathic megaesophagus.Mammalian genome : official journal of the International Mammalian Genome Society · 2023Article
- hPSC-derived sacral neural crest enables rescue in a severe model of Hirschsprung's disease.Cell stem cell · 2023Article
- The interplay of common genetic variants NRG1 rs2439302 and RET rs2435357 increases the risk of developing Hirschsprung's disease.Frontiers in cell and developmental biology · 2023Article
- Pathogenicity of p.Phe147del in RET in familial Hirschsprung's disease.American journal of translational research · 2023Article
- Development of the Gastrointestinal Tract in Newborns as a Challenge for an Appropriate Nutrition: A Narrative Review.Nutrients · 2022Review
- "Going the Extra Mile": A Sox10 Target, Cdh19, is Required for Sacral NC Migration in ENS Development.Gastroenterology · 2022Article
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Authors and funding
12 authors at 7 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimsThe enteric nervous system, which regulates many gastrointestinal functions, is derived from neural crest cells (NCCs). Defective NCC migration during embryonic development may lead to enteric neuropathies such as Hirschsprung's disease (hindgut aganglionosis). Sox10 is known to be essential for cell migration but downstream molecular events regulating early NCC migration have not been fully elucidated. This study aimed to determine how Sox10 regulates migration of sacral NCCs toward the hindgut using Dominant megacolon mice, an animal model of Hirschsprung's disease with a Sox10 mutation.
methodsWe used the following: time-lapse live cell imaging to determine the migration defects of mutant sacral NCCs; genome-wide microarrays, site-directed mutagenesis, and whole embryo culture to identify Sox10 targets; and liquid chromatography and tandem mass spectrometry to ascertain downstream effectors of Sox10.
resultsSacral NCCs exhibited retarded migration to the distal hindgut in Sox10-null embryos with simultaneous down-regulated expression of cadherin-19 (Cdh19). Sox10 was found to bind directly to the Cdh19 promoter. Cdh19 knockdown resulted in retarded sacral NCC migration in vitro and ex vivo, whereas re-expression of Cdh19 partially rescued the retarded migration of mutant sacral NCCs in vitro. Cdh19 formed cadherin-catenin complexes, which then bound to filamentous actin of the cytoskeleton during cell migration.
conclusionsCdh19 is a direct target of Sox10 during early sacral NCC migration toward the hindgut and forms cadherin-catenin complexes which interact with the cytoskeleton in migrating cells. Elucidation of this novel molecular pathway helps to provide insights into the pathogenesis of enteric nervous system developmental defects.
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