Epigenetic chromatin states uniquely define the developmental plasticity of murine hematopoietic stem cells.
(2010) In Blood 115. p.247-256- Abstract
- Heritable epigenetic signatures are proposed to serve as an important regulatory mechanism in lineage fate determination. To investigate this, we profiled chromatin modifications in murine hematopoietic stem cells, lineage restricted progenitors and CD4(+) T cells using modified genome-scale miniChIP technology. We show that genes involved in mature hematopoietic cell function associate with distinct chromatin states in stem and progenitor cells, prior to their activation or silencing upon cellular maturation. Many lineage-restricted promoters are associated with bivalent histone methylation and highly combinatorial histone modification patterns, which may determine their selective priming of gene expression during lineage commitment.... (More)
- Heritable epigenetic signatures are proposed to serve as an important regulatory mechanism in lineage fate determination. To investigate this, we profiled chromatin modifications in murine hematopoietic stem cells, lineage restricted progenitors and CD4(+) T cells using modified genome-scale miniChIP technology. We show that genes involved in mature hematopoietic cell function associate with distinct chromatin states in stem and progenitor cells, prior to their activation or silencing upon cellular maturation. Many lineage-restricted promoters are associated with bivalent histone methylation and highly combinatorial histone modification patterns, which may determine their selective priming of gene expression during lineage commitment. These bivalent chromatin states are conserved in mammalian evolution, with a particular over-representation of promoters encoding key regulators of hematopoiesis. Following differentiation into progenitors and T cells, activating histone modifications persist at transcriptionally repressed promoters, suggesting that these transcriptional programs might be reactivated after lineage restriction. Collectively, our data reveal the epigenetic framework that underlies the cell fate options of hematopoietic stem cells. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1512277
- author
- Weishaupt, Holger LU ; Sigvardsson, Mikael LU and Attema, Joanne LU
- organization
- publishing date
- 2010
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Blood
- volume
- 115
- pages
- 247 - 256
- publisher
- American Society of Hematology
- external identifiers
-
- wos:000273622600014
- pmid:19887676
- scopus:75649147458
- pmid:19887676
- ISSN
- 1528-0020
- DOI
- 10.1182/blood-2009-07-235176
- language
- English
- LU publication?
- yes
- id
- 48d3318a-16e3-4be6-a7be-2acaee38eb15 (old id 1512277)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/19887676?dopt=Abstract
- date added to LUP
- 2016-04-04 07:13:49
- date last changed
- 2022-05-09 00:27:19
@article{48d3318a-16e3-4be6-a7be-2acaee38eb15,
abstract = {{Heritable epigenetic signatures are proposed to serve as an important regulatory mechanism in lineage fate determination. To investigate this, we profiled chromatin modifications in murine hematopoietic stem cells, lineage restricted progenitors and CD4(+) T cells using modified genome-scale miniChIP technology. We show that genes involved in mature hematopoietic cell function associate with distinct chromatin states in stem and progenitor cells, prior to their activation or silencing upon cellular maturation. Many lineage-restricted promoters are associated with bivalent histone methylation and highly combinatorial histone modification patterns, which may determine their selective priming of gene expression during lineage commitment. These bivalent chromatin states are conserved in mammalian evolution, with a particular over-representation of promoters encoding key regulators of hematopoiesis. Following differentiation into progenitors and T cells, activating histone modifications persist at transcriptionally repressed promoters, suggesting that these transcriptional programs might be reactivated after lineage restriction. Collectively, our data reveal the epigenetic framework that underlies the cell fate options of hematopoietic stem cells.}},
author = {{Weishaupt, Holger and Sigvardsson, Mikael and Attema, Joanne}},
issn = {{1528-0020}},
language = {{eng}},
pages = {{247--256}},
publisher = {{American Society of Hematology}},
series = {{Blood}},
title = {{Epigenetic chromatin states uniquely define the developmental plasticity of murine hematopoietic stem cells.}},
url = {{http://dx.doi.org/10.1182/blood-2009-07-235176}},
doi = {{10.1182/blood-2009-07-235176}},
volume = {{115}},
year = {{2010}},
}