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Sequential EMT-MET induces neuronal conversion through Sox2.

Songwei He1,2,3, Jinlong Chen1,2,3, Yixin Zhang1,2,3

  • 1CAS Key Laboratory of Regenerative Biology, Joint School of Life Sciences, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou Medical University, Guangzhou, China.

Cell Discovery
|June 6, 2017
PubMed
Summary
This summary is machine-generated.

Sox2 drives a sequential epithelial-mesenchymal transition (EMT) to mesenchymal-epithelial transition (MET) switch, essential for converting mouse embryonic fibroblasts (MEFs) into neurons. This Sox2-mediated EMT-MET process is key for direct cell fate conversion.

Keywords:
Sox2TuJ+ cellsproliferationsequential EMT-MET

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Area of Science:

  • Cell biology
  • Developmental biology
  • Stem cell research

Background:

  • Direct neuronal conversion offers a promising avenue for regenerative medicine and disease modeling.
  • Understanding the molecular mechanisms driving cell fate transitions is crucial for improving conversion efficiency.

Purpose of the Study:

  • To elucidate the role of the epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) in direct neuronal conversion.
  • To investigate the function of Sox2 in mediating these transitions during the conversion of mouse embryonic fibroblasts (MEFs) to neurons.

Main Methods:

  • Utilized a defined 5C medium for inducing neuronal conversion from MEFs.
  • Analyzed the temporal dynamics of EMT and MET during the induction phase.
  • Investigated the role of Sox2, insulin, and basic fibroblast growth factor (bFGF) in the conversion process.
  • Assessed the impact of inhibiting EMT-MET stages on neuronal conversion.

Main Results:

  • A sequential EMT-MET process, orchestrated by Sox2, was identified as essential for MEF to TuJ+ cell conversion.
  • Early-stage proliferation (insulin, bFGF) induced EMT, up-regulated Stat3 and Sox2, and initiated neuronal differentiation.
  • Late-stage Sox2 activation promoted MET, directing cells towards a neuronal fate.
  • Sox2 could substitute for the sequential EMT-MET process in high-proliferation contexts, demonstrating its pivotal role.

Conclusions:

  • The sequential EMT-MET process is a critical and sufficient mechanism for direct neuronal conversion.
  • Sox2 plays a central role in orchestrating this EMT-MET switch, driving cell fate conversion.
  • These findings have implications for understanding cell plasticity in development, reprogramming, and cancer progression.