Research
Defining the chromatin signature of inducible genes in T cells
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* Corresponding author: Mary F Shannon frances.shannon@anu.edu.au
- † Equal contributors
1 Genome Biology Program and ACRF Biomolecular Resource Facility, John Curtin School of Medical Research, The Australian National University, Garran Road, Acton, ACT 0200, Australia
2 Current address: Department of Medicine/Hematology-Oncology, Weill Cornell Medical College, 68th St, New York, NY 10065, USA
3 Current address: Departments of Physiology and Pathology, National Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences and School of Basic Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, 1 Shuaifuyuan, Beijing 100730, PR China
Genome Biology 2009, 10:R107 doi:10.1186/gb-2009-10-10-r107
Published: 6 October 2009Abstract
Background
Specific chromatin characteristics, especially the modification status of the core histone proteins, are associated with active and inactive genes. There is growing evidence that genes that respond to environmental or developmental signals may possess distinct chromatin marks. Using a T cell model and both genome-wide and gene-focused approaches, we examined the chromatin characteristics of genes that respond to T cell activation.
Results
To facilitate comparison of genes with similar basal expression levels, we used expression-profiling data to bin genes according to their basal expression levels. We found that inducible genes in the lower basal expression bins, especially rapidly induced primary response genes, were more likely than their non-responsive counterparts to display the histone modifications of active genes, have RNA polymerase II (Pol II) at their promoters and show evidence of ongoing basal elongation. There was little or no evidence for the presence of active chromatin marks in the absence of promoter Pol II on these inducible genes. In addition, we identified a subgroup of genes with active promoter chromatin marks and promoter Pol II but no evidence of elongation. Following T cell activation, we find little evidence for a major shift in the active chromatin signature around inducible gene promoters but many genes recruit more Pol II and show increased evidence of elongation.
Conclusions
These results suggest that the majority of inducible genes are primed for activation by having an active chromatin signature and promoter Pol II with or without ongoing elongation.