The mammalian face is assembled in utero in a series of complex and interdependent molecular, cell and tissue processes. The orofacial complex appears to be exquisitely sensitive to genetic and environmental influence and this explains why clefts of the lip and palate are the most common congenital anomaly in humans (one in 700 live births). In this study, microarray technology was used to identify genes that may play pivotal roles in normal murine palatogenesis. mRNA was isolated from murine embryonic palatal shelves oriented vertically (before elevation), horizontally (following elevation, before contact), and following fusion. Changes in gene expression between the three different stages were analyzed with GeneChip microarrays. A number of genes were upregulated or downregulated, and large changes were seen in the expression of loricrin, glutamate decarboxylase, gamma-amino butyric acid type A receptor beta3 subunit, frizzled, Wnt-5a, metallothionein, annexin VIII, LIM proteins, Sox1, plakophilin1, cathepsin K and creatine kinase. In this paper, the changes in genetic profile of the developing murine palate are presented, and the possible role individual genes/proteins may play during normal palate development are discussed. Candidate genes with a putative role in cleft palate are also highlighted.

Download full-text PDF

Source
http://dx.doi.org/10.1034/j.1600-0854.2004.00686.xDOI Listing

Publication Analysis

Top Keywords

murine palatogenesis
8
normal palate
8
palate development
8
palate
5
microarray analysis
4
murine
4
analysis murine
4
palatogenesis temporal
4
temporal expression
4
genes
4

Similar Publications

MLL4 regulates postnatal palate growth and midpalatal suture development.

bioRxiv

November 2024

Department of Oral Biology, School of Dental Medicine, University at Buffalo, The State University of New York, Buffalo, NY 14214, U.S.A.

MLL4, also known as KMT2D, is a histone methyltransferase that acts as an important epigenetic regulator in various organogenesis programs. Mutations in the gene are the major cause of Kabuki syndrome, a human developmental disorder that involves craniofacial birth defects, including anomalies in the palate. This study aimed to investigate the role of MLL4 and the underlying mechanisms in the development and growth of the palate.

View Article and Find Full Text PDF

Background: Embryonic craniofacial development involves several cellular and molecular events that are evolutionarily conserved among vertebrates. Vertebrate models such as mice and zebrafish have been used to investigate the molecular and cellular etiologies underlying human craniofacial disorders, including orofacial clefts. However, the molecular mechanisms underlying embryonic development in these two species are unknown.

View Article and Find Full Text PDF

Identification of competing endogenous RNA networks associated with circRNA and lncRNA in TCDD-induced cleft palate development.

Toxicol Lett

November 2024

Center for Clinical Single-Cell Biomedicine, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou 450003, China. Electronic address:

Article Synopsis
  • TCDD, a teratogen, can cause cleft palates by impacting fetal development, and its mechanisms through competing endogenous RNAs (ceRNAs) like circRNAs and lncRNAs need further study.
  • A mouse model was used to analyze how TCDD affects palatal development, revealing significant changes in various RNA types and highlighting key pathways involved, specifically those related to the cytochrome P450 enzymes and aryl hydrocarbon receptor (AhR).
  • Two specific ceRNA networks, circRNA_1781/miR-30c-1-3p/PKIB and XR_380026.2/miR-1249-3p/DNAH10, were identified as critical players in palatal formation
View Article and Find Full Text PDF

Functional analysis of ESRP1/2 gene variants and CTNND1 isoforms in orofacial cleft pathogenesis.

Commun Biol

August 2024

Center for Craniofacial Innovation, Division of Plastic and Reconstructive Surgery, Department of Surgery, Children's Hospital of Philadelphia, Philadelphia, PA, USA.

Orofacial cleft (OFC) is a common human congenital anomaly. Epithelial-specific RNA splicing regulators ESRP1 and ESRP2 regulate craniofacial morphogenesis and their disruption result in OFC in zebrafish, mouse and humans. Using esrp1/2 mutant zebrafish and murine Py2T cell line models, we functionally tested the pathogenicity of human ESRP1/2 gene variants.

View Article and Find Full Text PDF

Cleft Palate Induced by Augmented Fibroblast Growth Factor-9 Signaling in Cranial Neural Crest Cells in Mice.

Stem Cells Dev

October 2024

Fujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatological Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, P.R. China.

Although enhanced fibroblast growth factor (FGF) signaling has been demonstrated to be crucial in many cases of syndromic cleft palate caused by tongue malposition in humans, animal models that recapitulate this phenotype are limited, and the precise mechanisms remain elusive. Mutations in with the effect of either loss- or gain-of-function effects have been identified to be associated with cleft palate in humans. Here, we generated a mouse model with a transgenic allele specifically activated in cranial neural crest cells, aiming to elucidate the gain-of-function effects of in palatogenesis.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!