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Related Experiment Videos

Developmental defects in mouse embryos lacking N-cadherin

G L Radice1, H Rayburn, H Matsunami

  • 1Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge 02139, USA. gradice@obgyn.upenn.edu

Developmental Biology
|January 1, 1997
PubMed
Summary
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N-cadherin is crucial for normal embryonic development, particularly heart formation. Gene mutation in mice led to malformed somites, neural tube defects, and severe heart abnormalities, proving N-cadherin

Area of Science:

  • Developmental Biology
  • Cell Adhesion
  • Molecular Biology

Background:

  • N-cadherin is an essential cell adhesion molecule.
  • Its precise in vivo functions during early embryogenesis are not fully understood.

Purpose of the Study:

  • To investigate the in vivo role of N-cadherin.
  • To elucidate the consequences of N-cadherin deficiency during mouse embryonic development.

Main Methods:

  • Generation of N-cadherin knockout mice.
  • Phenotypic analysis of homozygous mutant embryos.
  • In vitro studies of cardiac myocytes from mutant embryos.

Main Results:

  • N-cadherin mutant embryos exhibit normal initial neurulation and somitogenesis, but develop malformed structures.

Related Experiment Videos

  • Defects include abnormal somite morphology, disrupted epithelial organization, neural tube undulation, and yolk sac separation.
  • Severe cardiac defects observed, with myocyte dissociation and failure of heart tube development.
  • In vitro, N-cadherin-deficient cardiac myocytes show loose aggregation and synchronous beating.

    • Conclusions:

    • N-cadherin is critical for early heart development.
    • It plays a significant role in other morphogenetic processes, including somitogenesis and neural tube formation.
    • Loss of N-cadherin leads to embryonic lethality by Day 10 of gestation.