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Related Experiment Video

Updated: Jun 12, 2026

Visualization of Craniofacial Development in the sox10: kaede Transgenic Zebrafish Line Using Time-lapse Confocal Microscopy
06:35

Visualization of Craniofacial Development in the sox10: kaede Transgenic Zebrafish Line Using Time-lapse Confocal Microscopy

Published on: September 30, 2013

Dithiocarbamates induce craniofacial abnormalities and downregulate sox9a during zebrafish development.

Antonius Leonardus van Boxtel1, Bart Pieterse, Peter Cenijn

  • 1Institute for Environmental Studies (IVM), VU University, Amsterdam, The Netherlands.

Toxicological Sciences : an Official Journal of the Society of Toxicology
|June 10, 2010
PubMed
Summary

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Dithiocarbamates (DTCs) cause birth defects by disrupting gene expression in developing zebrafish. This study identifies a key gene, sox9a, involved in craniofacial development, offering insights into DTC teratogenesis.

Area of Science:

  • Developmental toxicology
  • Molecular biology
  • Zebrafish models

Background:

  • Dithiocarbamates (DTCs) are widely used but their teratogenic mechanisms are unclear.
  • Vertebrate development is sensitive to DTC exposure, causing abnormalities.

Purpose of the Study:

  • Investigate DTC teratogenesis mechanisms using zebrafish.
  • Identify molecular pathways affected by DTCs during development.

Main Methods:

  • Exposed zebrafish embryos and cells to DTCs (thiram, disulfiram, metam).
  • Analyzed gene expression changes using microarrays.
  • Examined sox9a expression in craniofacial structures.

Main Results:

  • Low nanomolar DTC exposure caused craniofacial abnormalities in zebrafish.

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  • Identified 166 differentially expressed genes, including those in connective tissue development.
  • Found downregulation of TGF-beta1 signaling genes, notably sox9a.
  • Observed perturbed sox9a expression in DTC-exposed zebrafish ceratobranchial arches.
  • Conclusions:

    • DTCs induce craniofacial abnormalities in zebrafish via disruption of gene networks.
    • sox9a downregulation is a key event in DTC-induced teratogenesis.
    • Provides a molecular basis for understanding DTC teratogenicity in vertebrates.