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Chromatin Immunoprecipitation (ChIP) in Mouse T-cell Lines
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Chromatin Immunoprecipitation (ChIP) in Mouse T-cell Lines

Published on: June 17, 2017

Differential control of Wnt target genes involves epigenetic mechanisms and selective promoter occupancy by T-cell

Simon Wöhrle1, Britta Wallmen, Andreas Hecht

  • 1Institute of Molecular Medicine and Cell Research, University of Freiburg, Stefan-Meier-Str. 17, D-79104 Freiburg, Germany.

Molecular and Cellular Biology
|October 10, 2007
PubMed

Insights

Wnt signaling relies on beta-catenin and TCF proteins to control gene activity. Specific TCF binding and epigenetic marks on Wnt target gene promoters dictate cellular responses.

Area of Science:

  • Molecular Biology
  • Epigenetics
  • Developmental Biology

Background:

  • Canonical Wnt signaling regulates gene expression via beta-catenin and T-cell factor (TCF) proteins.
  • Precise control of distinct genetic programs necessitates context-dependent gene activation or silencing.
  • The mechanisms by which beta-catenin and TCFs achieve selective gene regulation remain unclear.

Purpose of the Study:

  • To investigate Wnt target gene activation patterns and TCF promoter occupancy in mouse cell models.
  • To elucidate the role of epigenetic modifications in Wnt signaling pathway regulation.
  • To understand how cell-type-specific Wnt target gene regulation is achieved.

Main Methods:

  • Analysis of Wnt target gene activation in different mouse cell culture models.
  • Examination of TCF DNA-binding protein occupancy at Wnt-responsive and nonresponsive promoters.
  • Assessment of epigenetic modifications including DNA methylation and histone marks (H3 acetylation, H3K4 trimethylation, H3K27 trimethylation).

Main Results:

  • Within a cell type, Wnt-responsive promoters are bound by specific TCF subsets, while nonresponsive promoters are unoccupied.
  • Wnt-responsive promoters exhibit DNA hypomethylation and active histone marks (H3 hyperacetylation, H3K4 trimethylation).
  • Inactive promoters show DNA hypermethylation, lack active histone marks, and may possess repressive H3K27 trimethylation, independent of Wnt pathway activity.

Conclusions:

  • Cell-type-specific Wnt target gene regulation involves multilayered control systems.
  • Epigenetic modifications of promoter chromatin play a crucial role in determining Wnt signaling susceptibility.
  • Differential promoter occupancy by distinct TCF proteins, coupled with epigenetic states, dictates gene activation or silencing in response to Wnt signaling.

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