Musashi-2 controls cell fate, lineage bias, and TGF-β signaling in HSCs

J Exp Med. 2014 Jan 13;211(1):71-87. doi: 10.1084/jem.20130736. Epub 2014 Jan 6.

Abstract

Hematopoietic stem cells (HSCs) are maintained through the regulation of symmetric and asymmetric cell division. We report that conditional ablation of the RNA-binding protein Msi2 results in a failure of HSC maintenance and engraftment caused by a loss of quiescence and increased commitment divisions. Contrary to previous studies, we found that these phenotypes were independent of Numb. Global transcriptome profiling and RNA target analysis uncovered Msi2 interactions at multiple nodes within pathways that govern RNA translation, stem cell function, and TGF-β signaling. Msi2-null HSCs are insensitive to TGF-β-mediated expansion and have decreased signaling output, resulting in a loss of myeloid-restricted HSCs and myeloid reconstitution. Thus, Msi2 is an important regulator of the HSC translatome and balances HSC homeostasis and lineage bias.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Base Sequence
  • Cell Division / physiology*
  • Cell Lineage / physiology
  • Colony-Forming Units Assay
  • DNA Primers / genetics
  • Flow Cytometry
  • Fluorescent Antibody Technique
  • Hematopoiesis / physiology*
  • Hematopoietic Stem Cells / metabolism*
  • Immunoprecipitation
  • Mice
  • Mice, Knockout
  • Microarray Analysis
  • Molecular Sequence Data
  • RNA-Binding Proteins / genetics
  • RNA-Binding Proteins / metabolism*
  • Real-Time Polymerase Chain Reaction
  • Sequence Analysis, RNA
  • Signal Transduction / physiology*

Substances

  • DNA Primers
  • Msi2h protein, mouse
  • RNA-Binding Proteins