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C/EBPbeta induces chromatin opening at a cell-type-specific enhancer.

Annette Plachetka1, Olesya Chayka, Carola Wilczek

  • 1Institut für Biochemie, Westfälische-Wilhelms-Universität Münster, Wilhelm-Klemm-Str. 2, D-48149 Münster, Germany.

Molecular and Cellular Biology
|January 16, 2008
PubMed
Summary

CCAAT/enhancer binding protein (C/EBP) beta initiates chromatin opening at the mim-1 enhancer, while Myb is required for transcription and promoter chromatin opening. This reveals distinct roles in gene activation.

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Area of Science:

  • Molecular Biology
  • Gene Regulation
  • Chromatin Dynamics

Background:

  • The chicken mim-1 gene's expression is restricted to the myelomonocytic lineage and is regulated by Myb and CCAAT/enhancer binding protein (C/EBP) factors.
  • Myb and C/EBPbeta bind to distinct cis elements (promoter and enhancer) of mim-1, which are DNase I hypersensitive in expressing cells.

Purpose of the Study:

  • To investigate the molecular mechanisms by which transcription factors access target sites in compacted chromatin.
  • To elucidate the distinct roles of Myb and C/EBPbeta in activating the silenced mim-1 gene in nonhematopoietic cells.

Main Methods:

  • Utilized the chicken mim-1 gene as a model system.
  • Investigated chromatin accessibility using DNase I hypersensitivity assays.
  • Studied gene transcription and chromatin opening in response to transcription factor expression.

Main Results:

  • C/EBPbeta alone initiates chromatin opening at the mim-1 enhancer without inducing transcription.
  • Myb is essential for mim-1 transcription, which is associated with chromatin opening at the promoter.
  • Ectopic expression of Myb and C/EBPbeta activates the normally silent mim-1 gene in fibroblasts.

Conclusions:

  • Identified a novel function for C/EBPbeta in initiating localized chromatin opening at specific regulatory regions.
  • Demonstrated that Myb and C/EBPbeta act through independent mechanisms to achieve mim-1 gene activation.
  • Highlighted the sequential roles of transcription factors in overcoming chromatin-mediated repression.