Macrophage development from HSCs requires PU.1-coordinated microRNA expression
The differentiation of HSCs into myeloid lineages requires the transcription factor PU.1. Whereas PU.1-dependent induction of myeloid-specific target genes has been intensively studied, negative regulation of stem cell or alternate lineage programs remains incompletely characterized. To test for suc...
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| Vydáno v: | Blood Ročník 118; číslo 8; s. 2275 |
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| Hlavní autoři: | , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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United States
25.08.2011
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| ISSN: | 1528-0020, 1528-0020 |
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| Abstract | The differentiation of HSCs into myeloid lineages requires the transcription factor PU.1. Whereas PU.1-dependent induction of myeloid-specific target genes has been intensively studied, negative regulation of stem cell or alternate lineage programs remains incompletely characterized. To test for such negative regulatory events, we searched for PU.1-controlled microRNAs (miRs) by expression profiling using a PU.1-inducible myeloid progenitor cell line model. We provide evidence that PU.1 directly controls expression of at least 4 of these miRs (miR-146a, miR-342, miR-338, and miR-155) through temporally dynamic occupation of binding sites within regulatory chromatin regions adjacent to their genomic coding loci. Ectopic expression of the most robustly induced PU.1 target miR, miR-146a, directed the selective differentiation of HSCs into functional peritoneal macrophages in mouse transplantation assays. In agreement with this observation, disruption of Dicer expression or specific antagonization of miR-146a function inhibited the formation of macrophages during early zebrafish (Danio rerio) development. In the present study, we describe a PU.1-orchestrated miR program that mediates key functions of PU.1 during myeloid differentiation. |
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| AbstractList | The differentiation of HSCs into myeloid lineages requires the transcription factor PU.1. Whereas PU.1-dependent induction of myeloid-specific target genes has been intensively studied, negative regulation of stem cell or alternate lineage programs remains incompletely characterized. To test for such negative regulatory events, we searched for PU.1-controlled microRNAs (miRs) by expression profiling using a PU.1-inducible myeloid progenitor cell line model. We provide evidence that PU.1 directly controls expression of at least 4 of these miRs (miR-146a, miR-342, miR-338, and miR-155) through temporally dynamic occupation of binding sites within regulatory chromatin regions adjacent to their genomic coding loci. Ectopic expression of the most robustly induced PU.1 target miR, miR-146a, directed the selective differentiation of HSCs into functional peritoneal macrophages in mouse transplantation assays. In agreement with this observation, disruption of Dicer expression or specific antagonization of miR-146a function inhibited the formation of macrophages during early zebrafish (Danio rerio) development. In the present study, we describe a PU.1-orchestrated miR program that mediates key functions of PU.1 during myeloid differentiation. The differentiation of HSCs into myeloid lineages requires the transcription factor PU.1. Whereas PU.1-dependent induction of myeloid-specific target genes has been intensively studied, negative regulation of stem cell or alternate lineage programs remains incompletely characterized. To test for such negative regulatory events, we searched for PU.1-controlled microRNAs (miRs) by expression profiling using a PU.1-inducible myeloid progenitor cell line model. We provide evidence that PU.1 directly controls expression of at least 4 of these miRs (miR-146a, miR-342, miR-338, and miR-155) through temporally dynamic occupation of binding sites within regulatory chromatin regions adjacent to their genomic coding loci. Ectopic expression of the most robustly induced PU.1 target miR, miR-146a, directed the selective differentiation of HSCs into functional peritoneal macrophages in mouse transplantation assays. In agreement with this observation, disruption of Dicer expression or specific antagonization of miR-146a function inhibited the formation of macrophages during early zebrafish (Danio rerio) development. In the present study, we describe a PU.1-orchestrated miR program that mediates key functions of PU.1 during myeloid differentiation.The differentiation of HSCs into myeloid lineages requires the transcription factor PU.1. Whereas PU.1-dependent induction of myeloid-specific target genes has been intensively studied, negative regulation of stem cell or alternate lineage programs remains incompletely characterized. To test for such negative regulatory events, we searched for PU.1-controlled microRNAs (miRs) by expression profiling using a PU.1-inducible myeloid progenitor cell line model. We provide evidence that PU.1 directly controls expression of at least 4 of these miRs (miR-146a, miR-342, miR-338, and miR-155) through temporally dynamic occupation of binding sites within regulatory chromatin regions adjacent to their genomic coding loci. Ectopic expression of the most robustly induced PU.1 target miR, miR-146a, directed the selective differentiation of HSCs into functional peritoneal macrophages in mouse transplantation assays. In agreement with this observation, disruption of Dicer expression or specific antagonization of miR-146a function inhibited the formation of macrophages during early zebrafish (Danio rerio) development. In the present study, we describe a PU.1-orchestrated miR program that mediates key functions of PU.1 during myeloid differentiation. |
| Author | Bonifer, Constanze Stumm, Jürgen Lenze, Dido Abdelilah-Seyfried, Salim Lagendijk, Anne Riemke, Pia Bakkers, Jeroen Heinz, Sven Hummel, Michael Hoogenkamp, Maarten Schönheit, Jörg Ghani, Saeed Rosenbauer, Frank |
| Author_xml | – sequence: 1 givenname: Saeed surname: Ghani fullname: Ghani, Saeed organization: Max-Delbrück-Center for Molecular Medicine, Berlin, Germany – sequence: 2 givenname: Pia surname: Riemke fullname: Riemke, Pia – sequence: 3 givenname: Jörg surname: Schönheit fullname: Schönheit, Jörg – sequence: 4 givenname: Dido surname: Lenze fullname: Lenze, Dido – sequence: 5 givenname: Jürgen surname: Stumm fullname: Stumm, Jürgen – sequence: 6 givenname: Maarten surname: Hoogenkamp fullname: Hoogenkamp, Maarten – sequence: 7 givenname: Anne surname: Lagendijk fullname: Lagendijk, Anne – sequence: 8 givenname: Sven surname: Heinz fullname: Heinz, Sven – sequence: 9 givenname: Constanze surname: Bonifer fullname: Bonifer, Constanze – sequence: 10 givenname: Jeroen surname: Bakkers fullname: Bakkers, Jeroen – sequence: 11 givenname: Salim surname: Abdelilah-Seyfried fullname: Abdelilah-Seyfried, Salim – sequence: 12 givenname: Michael surname: Hummel fullname: Hummel, Michael – sequence: 13 givenname: Frank surname: Rosenbauer fullname: Rosenbauer, Frank |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21730352$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Animals Cell Differentiation - genetics Cell Line Cell Lineage - genetics Hematopoietic Stem Cells - cytology Hematopoietic Stem Cells - metabolism In Vitro Techniques Macrophages, Peritoneal - cytology Macrophages, Peritoneal - metabolism Mice Mice, Inbred C57BL MicroRNAs - genetics Myelopoiesis - genetics Proto-Oncogene Proteins - antagonists & inhibitors Proto-Oncogene Proteins - genetics RNA, Small Interfering - genetics Trans-Activators - antagonists & inhibitors Trans-Activators - genetics Zebrafish - embryology Zebrafish - genetics |
| Title | Macrophage development from HSCs requires PU.1-coordinated microRNA expression |
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