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Identification of the dysregulated let-7c-Sox2 network in the facial prominences of mouse embryos with early retinoid acid exposure

  • 0School of Life Science and Technology, Jinan University, Guangzhou, China.
Developmental Biology +

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April 3, 2025

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April 3, 2025

View abstract on PubMed

Summary

This summary is machine-generated.

Retinoic acid (RA) exposure disrupts embryonic development, altering let-7c and Sox2 expression. This dysregulation in facial development can lead to congenital malformations like cleft palate.

Area Of Science

  • Developmental Biology
  • Molecular Biology
  • Teratology

Background

  • Retinoic acid (RA) signaling is essential for embryonic development, particularly neural crest induction and craniofacial patterning.
  • Aberrant RA signaling is linked to congenital malformations such as cleft lip and palate in humans and animal models.

Purpose Of The Study

  • To investigate the molecular mechanisms underlying RA-induced craniofacial developmental defects.
  • To identify key regulatory networks affected by altered retinoic acid signaling during embryonic facial development.

Main Methods

  • Analysis of transcriptomic profiles in RA-exposed mouse embryos.
  • In vitro validation of regulatory interactions using luciferase assays.
  • Assessment of cell proliferation in response to altered gene expression.

Main Results

  • Early RA exposure dysregulated the let-7c-Sox2 network in embryonic facial prominences.
  • Increased let-7c expression and decreased Sox2 expression were observed in RA-treated embryos.
  • Reduced Sox2 expression correlated with hypoplasia and oral adhesion of palatal shelves, partly due to let-7c-mediated inhibition of mesenchymal proliferation.

Conclusions

  • The let-7c-Sox2 network is a critical target of retinoic acid signaling during craniofacial development.
  • Dysregulation of this network contributes to developmental abnormalities, including palatal hypoplasia and cleft palate.
  • Understanding these molecular pathways offers insights into the etiology of congenital facial malformations.

Keywords: