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Article: The role of the chromatin remodeler Mi-2β in hematopoietic stem cell self-renewal and multilineage differentiation

TitleThe role of the chromatin remodeler Mi-2β in hematopoietic stem cell self-renewal and multilineage differentiation
Authors
Issue Date2008
PublisherCold Spring Harbor Laboratory Press. The Journal's web site is located at http://genesdev.cshlp.org/
Citation
Genes And Development, 2008, v. 22 n. 9, p. 1174-1189 How to Cite?
AbstractThe ability of somatic stem cells to self-renew and differentiate into downstream lineages is dependent on specialized chromatin environments that keep stem cell-specific genes active and key differentiation factors repressed but poised for activation. The epigenetic factors that provide this type of regulation remain ill-defined. Here we provide the first evidence that the SNF2-like ATPase Mi-2β of the Nucleosome Remodeling Deacetylase (NuRD) complex is required for maintenance of and multilineage differentiation in the early hematopoietic hierarchy. Shortly after conditional inactivation of Mi-2β, there is an increase in cycling and a decrease in quiescence in an HSC (hematopoietic stem cell)-enriched bone marrow population. These cycling mutant cells readily differentiate into the erythroid lineage but not into the myeloid and lymphoid lineages. Together, these effects result in an initial expansion of mutant HSC and erythroid progenitors that are later depleted as more differentiated proerythroblasts accumulate at hematopoietic sites exhibiting features of erythroid leukemia. Examination of gene expression in the mutant HSC reveals changes in the expression of genes associated with self-renewal and lineage priming and a pivotal role of Mi-2β in their regulation. Thus, Mi-2β provides the hematopoietic system with immune cell capabilities as well as with an extensive regenerative capacity. © 2008 by Cold Spring Harbor Laboratory Press.
Persistent Identifierhttp://hdl.handle.net/10722/180732
ISSN
2015 Impact Factor: 10.042
2015 SCImago Journal Rankings: 11.812
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYoshida, Ten_US
dc.contributor.authorHazan, Ien_US
dc.contributor.authorZhang, Jen_US
dc.contributor.authorNg, SYen_US
dc.contributor.authorNaito, Ten_US
dc.contributor.authorSnippert, HJen_US
dc.contributor.authorHeller, EJen_US
dc.contributor.authorQi, Xen_US
dc.contributor.authorLawton, LNen_US
dc.contributor.authorWilliams, CJen_US
dc.contributor.authorGeorgopoulos, Ken_US
dc.date.accessioned2013-01-28T01:42:06Z-
dc.date.available2013-01-28T01:42:06Z-
dc.date.issued2008en_US
dc.identifier.citationGenes And Development, 2008, v. 22 n. 9, p. 1174-1189en_US
dc.identifier.issn0890-9369en_US
dc.identifier.urihttp://hdl.handle.net/10722/180732-
dc.description.abstractThe ability of somatic stem cells to self-renew and differentiate into downstream lineages is dependent on specialized chromatin environments that keep stem cell-specific genes active and key differentiation factors repressed but poised for activation. The epigenetic factors that provide this type of regulation remain ill-defined. Here we provide the first evidence that the SNF2-like ATPase Mi-2β of the Nucleosome Remodeling Deacetylase (NuRD) complex is required for maintenance of and multilineage differentiation in the early hematopoietic hierarchy. Shortly after conditional inactivation of Mi-2β, there is an increase in cycling and a decrease in quiescence in an HSC (hematopoietic stem cell)-enriched bone marrow population. These cycling mutant cells readily differentiate into the erythroid lineage but not into the myeloid and lymphoid lineages. Together, these effects result in an initial expansion of mutant HSC and erythroid progenitors that are later depleted as more differentiated proerythroblasts accumulate at hematopoietic sites exhibiting features of erythroid leukemia. Examination of gene expression in the mutant HSC reveals changes in the expression of genes associated with self-renewal and lineage priming and a pivotal role of Mi-2β in their regulation. Thus, Mi-2β provides the hematopoietic system with immune cell capabilities as well as with an extensive regenerative capacity. © 2008 by Cold Spring Harbor Laboratory Press.en_US
dc.languageengen_US
dc.publisherCold Spring Harbor Laboratory Press. The Journal's web site is located at http://genesdev.cshlp.org/en_US
dc.relation.ispartofGenes and Developmenten_US
dc.subject.meshAdenosine Triphosphatases - Genetics - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntigens, Cd - Analysisen_US
dc.subject.meshAntigens, Cd34 - Analysisen_US
dc.subject.meshApoptosisen_US
dc.subject.meshBone Marrow Cells - Cytology - Metabolismen_US
dc.subject.meshCell Cycleen_US
dc.subject.meshCell Differentiation - Genetics - Physiologyen_US
dc.subject.meshCell Lineageen_US
dc.subject.meshCell Proliferationen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshChromatin - Metabolismen_US
dc.subject.meshDna Helicasesen_US
dc.subject.meshErythrocytes - Cytology - Metabolismen_US
dc.subject.meshFemaleen_US
dc.subject.meshFlow Cytometry - Methodsen_US
dc.subject.meshGene Expression Profilingen_US
dc.subject.meshHematopoietic Stem Cells - Cytology - Metabolismen_US
dc.subject.meshLymphocytes - Cytology - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Knockouten_US
dc.subject.meshMyeloid Cells - Cytology - Metabolismen_US
dc.subject.meshOligonucleotide Array Sequence Analysis - Methodsen_US
dc.subject.meshReceptors, Transferrin - Analysisen_US
dc.titleThe role of the chromatin remodeler Mi-2β in hematopoietic stem cell self-renewal and multilineage differentiationen_US
dc.typeArticleen_US
dc.identifier.emailZhang, J: jzhang1@hku.hken_US
dc.identifier.authorityZhang, J=rp01713en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1101/gad.1642808en_US
dc.identifier.pmid18451107-
dc.identifier.scopuseid_2-s2.0-43249083123en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-43249083123&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume22en_US
dc.identifier.issue9en_US
dc.identifier.spage1174en_US
dc.identifier.epage1189en_US
dc.identifier.isiWOS:000255504500008-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridYoshida, T=7501316871en_US
dc.identifier.scopusauthoridHazan, I=6603277583en_US
dc.identifier.scopusauthoridZhang, J=22137260600en_US
dc.identifier.scopusauthoridNg, SY=16028784500en_US
dc.identifier.scopusauthoridNaito, T=7202253732en_US
dc.identifier.scopusauthoridSnippert, HJ=24175185800en_US
dc.identifier.scopusauthoridHeller, EJ=7103003041en_US
dc.identifier.scopusauthoridQi, X=7202430446en_US
dc.identifier.scopusauthoridLawton, LN=36880474100en_US
dc.identifier.scopusauthoridWilliams, CJ=35515772100en_US
dc.identifier.scopusauthoridGeorgopoulos, K=7006021598en_US

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