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Published on: January 26, 2018
Histone hyperacetylation within the beta-globin locus is context-dependent and precedes high-level gene expression
George Fromm1, Christina de Vries, Rachel Byron
1Departments of Pediatrics, Center for Pediatric Biomedical Research, University of Rochester Medical Center, Box 703, 601 Elmwood Ave, Rochester, NY14642, USA. Michael_bulger@urmc.rochester.edu
Blood
|August 20, 2009
Summary
Hyperacetylated domains, large regions of histone hyperacetylation, form early in gene regulation, independent of gene promoters or locus control regions. These domains are maintained even when transcription is inhibited.
Area of Science:
- Epigenetics
- Gene Regulation
- Chromatin Biology
Background:
- Active gene promoters feature histone modifications like hyperacetylation, influencing chromatin structure and transcription factor binding.
- Histone hyperacetylation can extend beyond promoters, forming large "hyperacetylated domains" whose formation and function are poorly understood.
Purpose of the Study:
- To investigate the mechanisms and timing of hyperacetylated domain formation at the murine beta-globin locus.
- To identify regulatory elements involved in establishing and maintaining these domains.
Main Methods:
- Analysis of histone modifications in murine beta-globin alleles with various genetic modifications (deletions).
- Assessment of domain formation relative to gene expression and cellular commitment stages.
Main Results:
- Hyperacetylated domain formation precedes high-level gene expression and erythroid commitment.
- Promoters and locus control regions are not essential for domain formation.
- Deletion of embryonic globin gene promoters induced domain formation in inactive definitive erythroid cells.
- Domains exhibit context-dependent hyperacetylation and are maintained despite inhibited transcriptional elongation.
Conclusions:
- Hyperacetylated domain formation is an early epigenetic event, potentially regulated by sequences within the locus itself.
- These domains are established independently of active transcription and promoter elements, suggesting novel regulatory mechanisms.
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