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Defining the chromatin signature of inducible genes in T cells

Lim, Pek S; Hardy, Kristine; Bunting, Karen; Ma, Lina; Peng, Kaiman; Chen, Xinxin; Shannon, Mary F

Description

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...[Show more]

dc.contributor.authorLim, Pek S
dc.contributor.authorHardy, Kristine
dc.contributor.authorBunting, Karen
dc.contributor.authorMa, Lina
dc.contributor.authorPeng, Kaiman
dc.contributor.authorChen, Xinxin
dc.contributor.authorShannon, Mary F
dc.date.accessioned2016-01-04T03:37:52Z
dc.date.available2016-01-04T03:37:52Z
dc.identifier.issn1465-6906
dc.identifier.urihttp://hdl.handle.net/1885/95207
dc.description.abstractBACKGROUND 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.
dc.publisherBioMed Central
dc.rights© 2009 Lim et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
dc.sourceGenome Biology
dc.subjectacetylation
dc.subjectbase composition
dc.subjectcd4-positive t-lymphocytes
dc.subjectchromatin
dc.subjectchromatin immunoprecipitation
dc.subjectcpg islands
dc.subjecthistones
dc.subjecthumans
dc.subjectlymphocyte activation
dc.subjectmethylation
dc.subjectpromoter regions, genetic
dc.subjectprotein binding
dc.subjectrna polymerase ii
dc.subjecttranscription, genetic
dc.subjectgene expression regulation
dc.titleDefining the chromatin signature of inducible genes in T cells
dc.typeJournal article
local.description.notesImported from ARIES
local.identifier.citationvolume10
dc.date.issued2009-10-06
local.identifier.absfor060199
local.identifier.ariespublicationu4020362xPUB162
local.publisher.urlhttp://www.biomedcentral.com/
local.type.statusPublished Version
local.contributor.affiliationLim, Pek (Chloe), College of Medicine, Biology and Environment, CMBE John Curtin School of Medical Research, Genome Sciences, The Australian National University
local.contributor.affiliationHardy, Kristine, College of Medicine, Biology and Environment, CMBE John Curtin School of Medical Research, Genome Sciences, The Australian National University
local.contributor.affiliationBunting, Karen L, Weill Cornell Medical College, United States of America
local.contributor.affiliationMa, Lina, College of Medicine, Biology and Environment, CMBE John Curtin School of Medical Research, Genome Sciences, The Australian National University
local.contributor.affiliationPeng, Kaiman, Institute of Basic Medical Sciences (Beijing), China
local.contributor.affiliationChen, Xinxin, Chinese Academy of Medical Sciences , China
local.contributor.affiliationShannon, M Frances, College of Medicine, Biology and Environment, CMBE John Curtin School of Medical Research, Genome Sciences, The Australian National University
local.identifier.essn1474-760X
local.bibliographicCitation.issue10
local.bibliographicCitation.startpageR107
local.bibliographicCitation.lastpage107.18
local.identifier.doi10.1186/gb-2009-10-10-r107
dc.date.updated2016-02-24T10:26:56Z
local.identifier.scopusID2-s2.0-75349108276
local.identifier.thomsonID000272227000009
CollectionsANU Research Publications

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