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Generation of Human Primordial Germ Cell-like Cells at the Surface of Embryoid Bodies from Primed-pluripotency Induced Pluripotent Stem Cells
12:06

Generation of Human Primordial Germ Cell-like Cells at the Surface of Embryoid Bodies from Primed-pluripotency Induced Pluripotent Stem Cells

Published on: January 11, 2019

Reprogramming primordial germ cells into pluripotent stem cells

Gabriela Durcova-Hills1, Fuchou Tang, Gina Doody

  • 1Wellcome Trust/Cancer Research UK Gurdon Institute of Cancer and Developmental Biology, University of Cambridge, Cambridge, United Kingdom. gd225@cam ac.uk

Plos One
|October 28, 2008
PubMed

Insights

Trichostatin A (TSA) can induce primordial germ cells (PGCs) to dedifferentiate into embryonic germ (EG) cells, replacing FGF-2. This process involves down-regulating Blimp1 and activating key reprogramming factors like c-Myc and Klf-4.

Area of Science:

  • Stem cell biology
  • Epigenetics
  • Cell fate determination

Background:

  • Primordial germ cell (PGC) specification establishes the germ cell lineage from pluripotent epiblast cells.
  • The Blimp1/Prmt5 complex is crucial for early germ cell lineage specification and maintenance.
  • Exogenous signaling molecules like FGF-2, LIF, and SCF can induce PGCs to dedifferentiate into embryonic germ (EG) cells.

Purpose of the Study:

  • To investigate Trichostatin A (TSA) as a potential inducer of PGC dedifferentiation.
  • To elucidate the molecular mechanisms underlying PGC dedifferentiation into EG cells.
  • To explore the role of Blimp1, c-Myc, Klf-4, and LIF/Stat-3 signaling in this process.

Main Methods:

  • Treatment of PGCs with Trichostatin A (TSA).
  • Analysis of gene expression changes, including Blimp1, c-Myc, and Klf-4.
  • Investigation of signaling pathway activation, specifically LIF/Stat-3.
  • Assessment of protein localization for Prmt5.

Main Results:

  • TSA effectively induces PGC dedifferentiation into EG cells, acting as a substitute for FGF-2.
  • A key event is the down-regulation of Blimp1, relieving its cell fate restriction.
  • Up-regulation of Blimp1 targets c-Myc and Klf-4, known reprogramming factors, was observed.
  • Early activation of the LIF/Stat-3 pathway and nuclear translocation of Stat-3 occurred.
  • Prmt5 translocated from the nucleus to the cytoplasm in EG cells.

Conclusions:

  • TSA is a potent agent for inducing PGC dedifferentiation into EG cells.
  • The down-regulation of Blimp1 and subsequent up-regulation of its targets are critical for this dedifferentiation process.
  • Understanding PGC dedifferentiation offers insights into the early mechanisms of cell reprogramming.
Abstract

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