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Gfi1 regulates miR-21 and miR-196b to control myelopoiesis

Velu, Chinavenmeni S., Baktula, Avinash M., Grimes, H. Leighton·2009·Blood
DOI 10.1182/blood-2008-11-190215
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Abstract

The zinc finger protein growth factor independent-1 (Gfi1) is a transcriptional repressor that is critically required for normal granulocytic differentiation. GFI1 loss-of-function mutations are found in some patients with severe congenital neutropenia (SCN). The SCN-associated GFI1-mutant proteins act as dominant negatives to block granulopoiesis through selective deregulation of a subset of GFI1 target genes. Here we show that Gfi1 is a master regulator of microRNAs, and that deregulated expression of these microRNAs recapitulates a Gfi1 loss-of-function block to granulocyte colony-stimulating factor (G-CSF)–stimulated granulopoiesis. Specifically, bone marrow cells from a GFI1-mutant SCN patient and Gfi1−/− mice display deregulated expression of miR-21 and miR-196B expression. Flow cytometric analysis and colony assays reveal that the overexpression or depletion of either miR induces changes in myeloid development. However, coexpression of miR-21 and miR-196b (as seen in Gfi1−/− mice and a GFI1N382S SCN patient) completely blocks G-CSF–induced granulopoiesis. Thus, our results not only identify microRNAs whose regulation is required during myelopoiesis, but also provide an example of synergy in microRNA biologic activity and illustrate potential mechanisms underlying SCN disease pathogenesis.

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Metadata

Authors
Velu, C. S., Baktula, A. M., & Grimes, H. L.
Affiliations
Division of Immunobiology, Cincinnati Children's Hospital Medical Center, OH
Venue
Blood
Publisher
American Society of Hematology
Published
2009-05-07
Volume
113
Issue
19
Pages
4720-4728
ISSN
  • 0006-4971
  • 1528-0020
DOI
10.1182/blood-2008-11-190215
Cited by
136
References
6
Language
en

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