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Craniofacial dysmorphogenesis in transgenic mice.

E D Kay1, S R Ross

  • 1Department of Pediatrics, College of Medicine, University of Illinois, Chicago 60612.

Journal of Craniofacial Genetics and Developmental Biology
|January 1, 1990
PubMed
Summary
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Transgenic mice carrying alpha-fetoprotein-chloramphenicol acetyl transferase (AFP-CAT) constructs developed craniofacial anomalies. The presence of the foreign CAT protein, not altered AFP levels, is implicated in causing these developmental defects.

Area of Science:

  • Developmental biology
  • Genetics
  • Toxicology

Background:

  • Alpha-fetoprotein (AFP) plays crucial roles in fetal development.
  • Transgenic technology allows for the study of gene regulation and function.
  • Investigating the impact of foreign gene expression on developmental processes is essential.

Purpose of the Study:

  • To investigate craniofacial anomalies observed in offspring of transgenic mice.
  • To determine the cause of these anomalies in relation to AFP-CAT transgenes.
  • To elucidate the role of the foreign CAT protein versus AFP levels in dysmorphogenesis.

Main Methods:

  • Generation of transgenic mice with alpha-fetoprotein-chloramphenicol acetyl transferase (AFP-CAT) constructs.
  • Crossbreeding transgenic mice with nontransgenic mates.

Related Experiment Videos

  • Detailed examination of craniofacial structures in affected fetuses.
  • Screening for the presence of the AFP-CAT transgene and assessment of AFP levels.
  • Main Results:

    • 11% of offspring from AFP-CAT transgenic crosses exhibited craniofacial anomalies.
    • Mandibular abnormalities were most common (92%), followed by zygomatic and ossicular defects (>40%).
    • Affected fetuses were heterozygous for the transgene, and normal AFP levels suggested the CAT protein's involvement.

    Conclusions:

    • The transgenic procedure, specifically the presence of the foreign CAT protein, is linked to craniofacial dysmorphogenesis.
    • The observed anomalies were not spontaneous but a consequence of transgene expression.
    • Further research is needed to fully understand the molecular mechanisms underlying these developmental defects.