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Neural tube, skeletal and body wall defects in mice lacking transcription factor AP-2.

The retinoic acid-inducible transcription factor AP-2 is expressed in epithelial and neural crest cell lineages during murine development. AP-2 can regulate neural and epithelial gene transcription, and is associated with overexpression of c-erbB-2 in human breast-cancer cell lines. To ascertain the importance of AP-2 for normal development, we have derived mice containing a homozygous disruption of the AP-2 gene. These AP-2-null mice have multiple congenital defects and die at birth. In particular, the AP-2 knockout mice exhibit anencephaly, craniofacial defects and thoraco-abdominoschisis. Skeletal defects occur in the head and trunk region, where many bones are deformed or absent. Analysis of these mice earlier in embryogenesis indicates a failure of cranial neural-tube closure and defects in cranial ganglia development. We have shown that AP-2 is a fundamental regulator of mammalian craniofacial development.

Pubmed ID: 8622766

Authors

  • Zhang J
  • Hagopian-Donaldson S
  • Serbedzija G
  • Elsemore J
  • Plehn-Dujowich D
  • McMahon AP
  • Flavell RA
  • Williams T

Journal

Nature

Publication Data

May 16, 1996

Associated Grants

None

Mesh Terms

  • Animals
  • Bone and Bones
  • Cranial Nerves
  • DNA-Binding Proteins
  • Female
  • Fetus
  • Immunoenzyme Techniques
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Muscles
  • Neural Crest
  • Neural Tube Defects
  • Skull
  • Transcription Factor AP-2
  • Transcription Factors