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RNA polymerase II progression through H3K27me3-enriched gene bodies requires JMJD3 histone demethylase

Conchi Estarás1, Raquel Fueyo, Naiara Akizu

  • 1Department of Molecular Genomics, Instituto de Biología Molecular de Barcelona, Consejo Superior de Investigaciones Científicas, 08028 Barcelona, Spain.

Molecular Biology of the Cell
|December 18, 2012
PubMed

Insights

JMJD3 (Jumonji domain-containing protein 3) facilitates gene transcription by removing H3K27me3 marks, enabling RNA polymerase II to progress along genes. This mechanism is crucial for transforming growth factor beta (TGFβ) signaling pathway activation.

Area of Science:

  • Molecular Biology
  • Epigenetics
  • Gene Regulation

Background:

  • JMJD3 is an H3K27me3 demethylase involved in transcriptional responses.
  • The precise mechanism by which JMJD3 facilitates transcription remains largely unknown.
  • Transforming growth factor beta (TGFβ) signaling pathway regulates numerous cellular processes.

Purpose of the Study:

  • To elucidate the mechanism by which JMJD3 regulates transcription.
  • To investigate JMJD3's role in TGFβ-responsive gene expression.
  • To understand how JMJD3 facilitates RNA polymerase II (RNAPII) progression.

Main Methods:

  • Chromatin immunoprecipitation followed by sequencing (ChIP-seq) to analyze JMJD3 and RNAPII localization.
  • Genome-wide analysis of JMJD3-dependent genes.
  • Molecular analyses to assess H3K27me3 demethylation and RNAPII progression.

Main Results:

  • JMJD3 and elongating RNAPII colocalize within gene bodies of TGFβ target genes upon TGFβ treatment.
  • JMJD3-dependent TGFβ target genes are enriched in H3K27me3 prior to pathway activation.
  • JMJD3 directly demethylates H3K27me3 along gene bodies, facilitating RNAPII progression.

Conclusions:

  • JMJD3 promotes transcriptional activation by removing H3K27me3 epigenetic marks.
  • This demethylation activity is essential for efficient RNAPII progression during TGFβ signaling.
  • The study reveals a key mechanism for JMJD3-mediated transcriptional regulation.

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