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Smad2 mediates Activin/Nodal signaling in mesendoderm differentiation of mouse embryonic stem cells

Teng Fei1, Shanshan Zhu, Kai Xia

  • 1The State Key Laboratory of Biomembrane and Membrane Biotechnology, School of Life Sciences, Tsinghua University, Beijing 100084, China.

Cell Research
|November 17, 2010
PubMed

Insights

Activin/Nodal signaling is not essential for mouse embryonic stem cell self-renewal but is crucial for mesendoderm differentiation. This pathway regulates key developmental genes, with Tapbp identified as a critical downstream mediator.

Area of Science:

  • Developmental Biology
  • Stem Cell Biology
  • Molecular Signaling

Background:

  • Activin/Nodal signaling is known to regulate human embryonic stem cell pluripotency.
  • Its precise role in mouse embryonic stem cells remains less understood.

Purpose of the Study:

  • To elucidate the function of Activin/Nodal signaling in mouse embryonic stem cells.
  • To identify downstream targets and mechanisms involved in mesendoderm differentiation.

Main Methods:

  • Confirmation of active Smad2-mediated Activin/Nodal signaling in mouse ES cells.
  • Genome-wide chromatin immunoprecipitation-chip (ChIP-chip) analysis to identify Smad2-bound genes.
  • Investigating the role of identified genes in mesendoderm differentiation.

Main Results:

  • Smad2-mediated Activin/Nodal signaling is dispensable for self-renewal but essential for mesendoderm differentiation.
  • Transcriptional correlation observed between Smad2 binding and signaling modulation.
  • Development-related genes were enriched among Smad2-bound targets.
  • Tapbp identified as a key downstream mediator in mesendoderm differentiation.

Conclusions:

  • Smad2-mediated Activin/Nodal signaling orchestrates mesendoderm lineage commitment in mouse ES cells.
  • This occurs through direct modulation of developmental regulator gene expression.
  • Tapbp plays a critical role downstream of this pathway.

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