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Related Experiment Videos

Maternal beta-catenin and E-cadherin in mouse development.

Wilhelmine N De Vries1, Alexei V Evsikov, Bryce E Haac

  • 1The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA.

Development (Cambridge, England)
|August 13, 2004
PubMed
Summary

Maternal E-cadherin is not essential for early mouse embryo development, but its absence, along with beta-catenin, impacts developmental success. This suggests E-cadherin influences nuclear beta-catenin during embryonic genome activation.

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Area of Science:

  • Developmental Biology
  • Cell Biology
  • Genetics

Background:

  • Oocyte to embryo transition relies on maternal factors for development initiation and embryonic genome activation.
  • Cell adhesion molecules, like E-cadherin and beta-catenin, play crucial roles in early embryonic development.

Purpose of the Study:

  • To investigate the role of maternal E-cadherin and beta-catenin in mouse oocyte-to-embryo transition.
  • To determine the necessity of early blastomere adhesion for embryonic development.

Main Methods:

  • Conditional elimination of maternal E-cadherin gene in mouse oocytes.
  • Partial elimination of maternal beta-catenin gene in mouse oocytes.
  • Observation of blastomere adhesion, compaction, and developmental progression.

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Main Results:

  • Embryos lacking maternal E-cadherin or expressing truncated beta-catenin showed impaired blastomere adhesion.
  • Adhesion was restored by paternal gene products, indicating adhesion is not critical in early stages.
  • Maternal E-cadherin absence alleviated developmental deficits caused by absent wild-type beta-catenin.

Conclusions:

  • Early blastomere adhesion is not essential for the oocyte-to-embryo transition in mice.
  • The zona pellucida maintains blastomere proximity until compaction occurs.
  • E-cadherin may regulate nuclear beta-catenin availability during embryonic genome activation.