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BAD regulates mammary gland morphogenesis by 4E-BP1-mediated control of localized translation in mouse and human

John Maringa Githaka1, Namita Tripathi1, Raven Kirschenman1

  • 1Department of Biochemistry, University of Alberta, Edmonton, AB, Canada.

Nature Communications
|May 20, 2021
PubMed

Insights

The Bcl-2 family member BAD regulates mammary gland development by controlling localized translation and cell migration. This protein is crucial for tubulogenesis and focal adhesion maturation during tissue homeostasis.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Molecular Biology

Background:

  • Non-canonical protein functions are key to understanding tissue homeostasis.
  • The Bcl-2 family member BAD's role in development is largely unexplored.

Purpose of the Study:

  • To investigate the function of BAD in postnatal mammary gland morphogenesis.
  • To elucidate the molecular mechanisms by which BAD influences tissue development.

Main Methods:

  • Utilized Bad 3SA knock-in mouse models.
  • Performed proteomic and Reverse-Phase Protein Array (RPPA) analyses.
  • Analyzed organoid models and cell migration assays.

Main Results:

  • BAD phosphorylation status impacts pubertal mammary gland development and ductal tubulogenesis.
  • BAD regulates focal adhesions and mRNA translation repressor 4E-BP1.
  • BAD deficiency leads to unstable protrusions, impaired localized translation, and reduced cell migration.

Conclusions:

  • BAD plays an unexpected role in controlling localized translation and cell migration.
  • BAD is essential for mammary gland development by modulating focal adhesion maturation and cell motility.
  • Targeting BAD-mediated pathways may offer new strategies for tissue regeneration and development.

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