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Light-mediated Reversible Modulation of the Mitogen-activated Protein Kinase Pathway during Cell Differentiation and Xenopus Embryonic Development
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A chromatin-modifying function of JNK during stem cell differentiation.

Vijay K Tiwari1, Michael B Stadler, Christiane Wirbelauer

  • 1Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland.

Nature Genetics
|December 20, 2011
PubMed
Summary

The c-Jun NH(2)-terminal kinase (JNK) pathway guides stem cell differentiation into neurons. JNK binds active promoters, phosphorylates histone H3 Ser10, and regulates gene expression during this process.

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Area of Science:

  • Cellular signaling and gene regulation
  • Stem cell differentiation and neurogenesis
  • Epigenetics and chromatin modification

Background:

  • Mitogen-activated protein (MAP) kinases, including the c-Jun NH(2)-terminal kinase (JNK) pathway, are involved in cellular responses.
  • While JNK's role in stress response is known, its mechanism in development, particularly stem cell differentiation, remains unclear.
  • Understanding JNK's function in neurogenesis is crucial for developmental biology and regenerative medicine.

Purpose of the Study:

  • To elucidate the mechanism by which the JNK pathway regulates stem cell differentiation into neurons.
  • To identify specific genomic targets of JNK during neurogenesis.
  • To investigate the role of JNK in chromatin modification and gene expression during stem cell development.

Main Methods:

  • Genome-wide location analysis to map JNK binding sites on chromatin during stem cell differentiation.
  • Analysis of transcription factor binding motifs (NF-Y, AP-1) at JNK-bound promoters.
  • Assessment of histone H3 Ser10 (H3S10) phosphorylation as a substrate for JNK.
  • Inhibition of JNK signaling to observe effects on H3S10 phosphorylation and target gene expression in post-mitotic neurons.

Main Results:

  • JNK binds to a large set of active promoters during stem cell differentiation into neurons.
  • JNK-bound promoters are enriched for NF-Y binding motifs, and NF-Y occupies these sites.
  • Histone H3 Ser10 (H3S10) is a direct substrate of JNK, and JNK-bound promoters show enrichment for H3S10 phosphorylation.
  • Inhibition of JNK signaling reduces H3S10 phosphorylation and target gene expression in neurons.

Conclusions:

  • The JNK pathway plays a critical role in regulating gene expression during stem cell differentiation into neurons.
  • JNK functions by binding to active promoters and phosphorylating histone H3 Ser10, thereby influencing chromatin state and gene transcription.
  • These findings reveal a novel mechanism of MAP kinase action on chromatin at a new class of target genes during stem cell development.