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Related Concept Videos

Pleiotropy01:33

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Pleiotropy is the phenomenon in which a single gene impacts multiple, seemingly unrelated phenotypic traits. For example, defects in the SOX10 gene cause Waardenburg Syndrome Type 4, or WS4, which can cause defects in pigmentation, hearing impairments, and an absence of intestinal contractions necessary for elimination. This diversity of phenotypes results from the expression pattern of SOX10 in early embryonic and fetal development. SOX10 is found in neural crest cells that form melanocytes,...
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The gene expression in cells is regulated at different stages: (i) transcription, (ii) RNA processing, (iii) RNA localization, and (iv) translation. Transcriptional regulation is mediated by regulatory proteins such as transcription factors, activators, or repressors—these control gene expression by initiating or inhibiting the transcription of genes. Once a precursor or pre-mRNA is produced, it undergoes post-transcriptional modification, including 5' capping, splicing, and the...
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Gene expression can be regulated at almost every step from gene to protein. Transcription is the step that is most commonly regulated. This involves the binding of proteins to short regulatory sequences on the DNA. This association can either promote or inhibit the transcription of a gene associated with the respective sequence.
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Updated: Dec 1, 2025

Tissue Preparation and Immunostaining of Mouse Craniofacial Tissues and Undecalcified Bone
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Med23 Regulates Sox9 Expression during Craniofacial Development.

S Dash1, S Bhatt1,2, K T Falcon1

  • 1Stowers Institute for Medical Research, Kansas City, MO, USA.

Journal of Dental Research
|November 6, 2020
PubMed
Summary
This summary is machine-generated.

Loss of Med23 in neural crest cells causes craniofacial defects like micrognathia and cleft palate. Med23 normally represses SOX9, a key factor in these developmental disorders.

Keywords:
MediatorPierre Robin sequencecleft palatecleidocranial dysplasiamicrognathianeural crest cells

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Area of Science:

  • Developmental Biology
  • Genetics
  • Molecular Biology

Background:

  • Craniofacial birth defects have complex causes, involving genetic and environmental factors.
  • Despite identifying many genes, the etiology of many craniofacial anomalies remains unknown.
  • Neural crest cells are crucial for craniofacial development.

Purpose of the Study:

  • To investigate the role of Mediator complex subunit protein Med23 in neural crest cells during craniofacial development.
  • To elucidate the molecular mechanisms underlying Med23's function in craniofacial morphogenesis.

Main Methods:

  • Conditional knockout of Med23 in mouse neural crest cells (Med23flox/flox;Wnt1-Cre).
  • Analysis of craniofacial phenotypes, including micrognathia, glossoptosis, and cleft palate.
  • Gene expression analysis (Sox9, Col2a1, Wnt signaling targets) and protein-protein interactions (Sox9-beta-catenin).
  • In vitro studies to assess Med23's regulation of Sox9 expression.

Main Results:

  • Med23 loss in neural crest cells phenocopies Pierre Robin sequence (micrognathia, glossoptosis, cleft palate).
  • Upregulation of SOX9 mRNA and protein in Med23-deficient embryos.
  • Med23 directly represses Sox9 expression by binding to its promoter.
  • Enhanced Sox9 binding to beta-catenin, decreased Wnt signaling, reduced proliferation, and altered jaw skeletal differentiation.

Conclusions:

  • Med23 is essential in neural crest cells for normal craniofacial development.
  • Med23 acts by repressing Sox9, influencing Wnt signaling and cell proliferation.
  • This study links the Mediator complex to the pathogenesis of craniofacial anomalies like micrognathia and cleft palate.