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Bone Marrow-derived Macrophage Production
07:06

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Published on: November 22, 2013

Jmjd3 contributes to the control of gene expression in LPS-activated macrophages

Francesca De Santa1, Vipin Narang, Zhei Hwee Yap

  • 1Department of Experimental Oncology, European Institute of Oncology (IEO), IFOM-IEO Campus, Milan, Italy.

The EMBO Journal
|September 26, 2009
PubMed

Insights

Jmjd3 fine-tunes inflammatory gene expression in macrophages. Its role in inflammatory gene transcription is independent of H3K27 demethylation, suggesting a novel regulatory mechanism.

Area of Science:

  • Epigenetics
  • Molecular Biology
  • Immunology

Background:

  • Jmjd3 is a histone demethylase induced by NF-kB in response to microbial stimuli.
  • Jmjd3 removes H3K27me3, a mark linked to gene repression and cell fate.
  • The precise role of Jmjd3 and H3K27me3 demethylation in inflammatory gene expression is unclear.

Purpose of the Study:

  • To investigate the contribution of Jmjd3 induction and H3K27me3 demethylation to inflammatory gene expression.
  • To determine the recruitment patterns of Jmjd3 in activated macrophages.
  • To elucidate the mechanism by which Jmjd3 regulates inflammatory gene transcription.

Main Methods:

  • Chromatin immunoprecipitation-sequencing (ChIP-seq) was used to identify Jmjd3 binding sites.
  • Analysis of Jmjd3 target genes and their regulation upon Jmjd3 deletion.
  • Assessment of RNA polymerase II (Pol_II) recruitment and gene transcription.

Main Results:

  • Jmjd3 preferentially binds to transcription start sites with high H3K4me3 and Pol_II.
  • Approximately 70% of lipopolysaccharide (LPS)-inducible genes are Jmjd3 targets.
  • Deletion of Jmjd3 moderately impaired Pol_II recruitment and transcription of a subset of genes, including inflammatory genes, independent of H3K27me3 levels.

Conclusions:

  • Jmjd3 fine-tunes the transcriptional output of LPS-activated macrophages.
  • The regulatory function of Jmjd3 in this context is independent of H3K27 demethylation.
  • Jmjd3 influences inflammatory gene expression through a mechanism not directly linked to H3K27me3 modification.

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