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Disabled-2 is essential for endodermal cell positioning and structure formation during mouse embryogenesis.

Dong-Hua Yang1, Elizabeth R Smith, Isabelle H Roland

  • 1Department of Medical Oncology, Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111, USA.

Developmental Biology
|November 5, 2002
PubMed
Summary
This summary is machine-generated.

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Signal Transduction Adapter Protein Disabled-2 (Dab2) is crucial for organizing visceral endoderm cells in early mouse development. Its absence leads to embryonic lethality due to failed cell positioning and structure formation.

Area of Science:

  • Developmental Biology
  • Cell Biology
  • Genetics

Background:

  • Disabled-2 (Dab2) is a signal transduction adapter protein and a mammalian ortholog of Drosophila Disabled.
  • Dab2 is widely expressed in epithelial cells, unlike its brain-specific homolog, Dab1.
  • Its role in early embryonic development was previously unclear.

Purpose of the Study:

  • To investigate the function of Dab2 in early mouse embryonic development.
  • To determine the consequences of Dab2 deficiency on embryonic structure and cell organization.
  • To elucidate the role of Dab2 in visceral endoderm formation and function.

Main Methods:

  • Generation of Dab2-deficient mice using gene targeting (LacZ insertion).
  • Analysis of Dab2 expression patterns during early embryogenesis (E4.5 onwards).

Related Experiment Videos

  • In vitro culture of Dab2-deficient blastocysts to assess early developmental defects.

    • Main Results:

    • Homozygous Dab2-deficient mutants are embryonic lethal before E6.5.
    • Defects in visceral endoderm cell positioning and organization are observed in Dab2 (-/-) conceptuses.
    • Failure of epiblast expansion and proamniotic cavity formation occurs in Dab2-deficient embryos.
    • In vitro, Dab2 (-/-) endodermal cells are disorganized, leading to inner cell mass growth failure and outgrowth degeneration.

    Conclusions:

    • Dab2 is essential for the proper organization of visceral endoderm cells during early mouse development.
    • The absence of an organized visceral endoderm in Dab2-deficient embryos results in inner cell mass growth failure.
    • Dab2 likely regulates endodermal cell organization via a signal pathway involving endocytosis of ligands from the blastocoel.