Macrophage development from HSCs requires PU.1-coordinated microRNA expression | Zendy

Saeed Ghani | Zendy; Pia Riemke | Zendy; Jörg Schönheit | Zendy; Dido Lenze | Zendy; Jürgen Stumm | Zendy; Maarten Hoogenkamp | Zendy; Anne K. Lagendijk | Zendy; Sven Heinz | Zendy; Constanze Bonifer | Zendy; Jeroen Bakkers | Zendy; Salim AbdelilahSeyfried | Zendy; Michael Hummel | Zendy; Frank Rosenbauer | Zendy

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Macrophage development from HSCs requires PU.1-coordinated microRNA expression

Author(s) -

Saeed Ghani,

Pia Riemke,

Jörg Schönheit,

Dido Lenze,

Jürgen Stumm,

Maarten Hoogenkamp,

Anne K. Lagendijk,

Sven Heinz,

Constanze Bonifer,

Jeroen Bakkers,

Salim AbdelilahSeyfried,

Michael Hummel,

Frank Rosenbauer

Publication year - 2011

Publication title -

blood

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 5.515

H-Index - 465

eISSN - 1528-0020

pISSN - 0006-4971

DOI - 10.1182/blood-2011-02-335141

Subject(s) - dicer , biology , ectopic expression , microrna , zebrafish , microbiology and biotechnology , myeloid , transcription factor , gene expression profiling , chromatin , stem cell , cellular differentiation , irf8 , transplantation , regulation of gene expression , gene expression , cancer research , genetics , rna interference , gene , rna , medicine , surgery

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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