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Updated: Feb 16, 2026

A Simple Method to Identify Kinases That Regulate Embryonic Stem Cell Pluripotency by High-throughput Inhibitor Screening
07:18

A Simple Method to Identify Kinases That Regulate Embryonic Stem Cell Pluripotency by High-throughput Inhibitor Screening

Published on: May 12, 2017

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Distinct SoxB1 networks are required for naïve and primed pluripotency

Andrea Corsinotti1,2, Frederick Ck Wong1, Tülin Tatar1

  • 1MRC Centre for Regenerative Medicine, Institute for Stem Cell Research, School of Biological Sciences, University of Edinburgh, Edinburgh, Scotland.

Elife
|December 20, 2017
PubMed

Insights

Sox2 deletion in mouse embryonic stem cells causes differentiation. However, epiblast stem cells tolerate Sox2 loss due to increased Sox3, revealing SOXB1 protein balance is critical for pluripotency and cell fate.

Area of Science:

  • Developmental Biology
  • Stem Cell Biology
  • Gene Regulation

Background:

  • Sox2 deletion in mouse embryonic stem cells (ESCs) induces trophectodermal differentiation.
  • The role of SOXB1 proteins (SOX1, SOX2, SOX3) in epiblast stem cell (EpiSC) pluripotency remains unclear.
  • SOXB1 proteins are crucial regulators of pluripotency and early embryonic development.

Purpose of the Study:

  • To investigate the function of SOXB1 proteins in epiblast stem cell pluripotency.
  • To determine the impact of altered SOXB1 expression balance on cell fate decisions.
  • To elucidate the differential roles of SOX2 and SOX3 in maintaining distinct pluripotent states.

Main Methods:

  • Genetic manipulation of Sox2 and Sox3 in mouse ESCs and EpiSCs.
  • Analysis of stem cell self-renewal and differentiation potential.
  • Quantitative assessment of SOXB1 protein expression levels.

Main Results:

  • Sox2 can be deleted from EpiSCs without affecting self-renewal, unlike in ESCs.
  • EpiSCs exhibit a distinct SOXB1 expression profile with decreased Sox2 and increased Sox3 compared to ESCs.
  • Deletion of both Sox2 and Sox3 in EpiSCs impairs self-renewal, indicating functional redundancy and critical combined roles.
  • Altered SOXB1 levels influence differentiation choices, with implications for the ESC to EpiSC transition and neural differentiation.

Conclusions:

  • Optimal SOXB1 protein levels are essential for maintaining specific pluripotent states (ESCs vs. EpiSCs).
  • A shift in the SOXB1 expression balance, particularly increased Sox3, compensates for Sox2 loss in EpiSCs.
  • SOXB1 proteins play critical, state-dependent roles in cell fate decisions during the exit from naive pluripotency.
Keywords:
Embryonic stem cellsEpiblast stem cellsPluripotencySoxdevelopmental biologymousestem cellstranscription factors

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