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Isolation and Derivation of Mouse Embryonic Germinal Cells
14:01

Isolation and Derivation of Mouse Embryonic Germinal Cells

Published on: October 22, 2009

AKT signaling promotes derivation of embryonic germ cells from primordial germ cells

Tohru Kimura1, Maya Tomooka, Noriko Yamano

  • 1Department of Pathology, Graduate School of Medicine, Osaka University, 2-2 Yamada-oka, Suita, Osaka, Japan.

Development (Cambridge, England)
|January 25, 2008
PubMed

Insights

Activating AKT signaling in primordial germ cells (PGCs) boosts their ability to become pluripotent embryonic germ (EG) cells. This effect is mediated by p53, highlighting AKT

Area of Science:

  • Developmental Biology
  • Stem Cell Biology
  • Molecular Biology

Background:

  • Primordial germ cells (PGCs) are precursors to germ cells but can gain pluripotency, forming embryonic germ (EG) cells or teratomas.
  • PTEN inactivation in PGCs enhances EG cell production and teratoma formation, indicating the PI3K/AKT pathway's role.
  • AKT is a key downstream effector of PI3K, but its specific role in PGC developmental potency requires elucidation.

Purpose of the Study:

  • To investigate the effect of AKT signaling activation on the developmental potency of primordial germ cells (PGCs).
  • To determine the downstream targets of AKT signaling that mediate changes in PGC pluripotency.
  • To explore AKT's role in the establishment of embryonic germ (EG) cells.

Main Methods:

  • Utilized transgenic mice expressing a ligand-regulatable AKT-MER fusion protein in PGCs.
  • Administered 4-hydroxytamoxifen to activate AKT signaling in PGCs at specific developmental stages.
  • Assessed the efficiency of embryonic germ (EG) cell establishment and analyzed molecular changes in PGCs, including protein phosphorylation and localization.

Main Results:

  • Hyperactivation of AKT signaling in proliferative PGCs significantly increased the efficiency of embryonic germ (EG) cell establishment.
  • AKT activation partially substituted for the requirement of bFGF, a crucial growth factor for EG cell derivation.
  • AKT activation in PGCs led to GSK3 phosphorylation, increased MDM2 stability and nuclear localization, and suppressed p53 phosphorylation.

Conclusions:

  • AKT signaling activation dramatically enhances the developmental potency of PGCs, particularly during proliferation, promoting EG cell establishment.
  • p53 deficiency recapitulates the effects of AKT hyperactivation on EG cell derivation, identifying p53 as a crucial downstream target of PI3K/AKT signaling in PGCs.
  • GSK3 inhibition is not a critical mediator of AKT's effects on PGC pluripotency, distinguishing it from p53's role.

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