ArticleBMC genomics2018
Identification of sonic hedgehog-regulated genes and biological processes in the cranial neural crest mesenchyme by comparative transcriptomics.
Article in BMC genomics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Overexpression of miR-320-3p, miR-381-3p, and miR-27a-3p Suppresses Genes Related to Midline Facial Cleft in Mouse Cranial Neural Crest Cells.International journal of molecular sciences · 2025Article
- Ripply3 overdosage induces mid-face shortening through Tbx1 downregulation in Down syndrome models.PLoS genetics · 2025Article
- Disruption of DNA methylation-mediated cranial neural crest proliferation and differentiation causes orofacial clefts in mice.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- TFAP2 paralogs regulate midfacial development in part through a conserved ALX genetic pathway.Development (Cambridge, England) · 2024Article
- High-throughput detection of craniofacial defects in fluorescent zebrafish.Birth defects research · 2023Article
- TGF-β signaling and Creb5 cooperatively regulate Fgf18 to control pharyngeal muscle development.eLife · 2022Article
- A Neural Crest-specific Overexpression Mouse Model Reveals the Transcriptional Regulatory Effects of Dlx2 During Maxillary Process Development.Frontiers in physiology · 2022Article
- Time-resolved proteomics profiling of the ciliary Hedgehog response.The Journal of cell biology · 2021Article
- Metformin upregulates the expression of Gli1 in vascular endothelial cells in hyperoxia-exposed neonatal mice.American journal of translational research · 2020Article
- Sonic Hedgehog Signaling in Cranial Neural Crest Cells Regulates Microvascular Morphogenesis in Facial Development.Frontiers in cell and developmental biology · 2020Article
- A radical switch in clonality reveals a stem cell niche in the epiphyseal growth plate.Nature · 2019Article
- Six NSCL/P Loci Show Associations With Normal-Range Craniofacial Variation.Frontiers in genetics · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe evolutionarily conserved Sonic Hedgehog (Shh) signaling pathway is essential for embryogenesis and orofacial development. SHH ligand secreted from the surface ectoderm activates pathway activity in the underlying cranial neural crest cell (cNCC)-derived mesenchyme of the developing upper lip and palate. Disruption of Shh signaling causes orofacial clefts, but the biological action of Shh signaling and the full set of Shh target genes that mediate normal and abnormal orofacial morphogenesis have not been described.
resultsUsing comparative transcriptional profiling, we have defined the Shh-regulated genes of the cNCC-derived mesenchyme. Enrichment analysis demonstrated that in cultured cNCCs, Shh-regulated genes are involved in smooth muscle and chondrocyte differentiation, as well as regulation of the Forkhead family of transcription factors, G1/S cell cycle transition, and angiogenesis. Next, this gene set from Shh-activated cNCCs in vitro was compared to the set of genes dysregulated in the facial primordia in vivo during the initial pathogenesis of Shh pathway inhibitor-induced orofacial clefting. Functional gene annotation enrichment analysis of the 112 Shh-regulated genes with concordant expression changes linked Shh signaling to interdependent and unique biological processes including mesenchyme development, cell adhesion, cell proliferation, cell migration, angiogenesis, perivascular cell markers, and orofacial clefting.
conclusionsWe defined the Shh-regulated transcriptome of the cNCC-derived mesenchyme by comparing the expression signatures of Shh-activated cNCCs in vitro to primordial midfacial tissues exposed to the Shh pathway inhibitor in vivo. In addition to improving our understanding of cNCC biology by determining the identity and possible roles of cNCC-specific Shh target genes, this study presents novel candidate genes whose examination in the context of human orofacial clefting etiology is warranted.
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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.