The RNA-binding protein QKI5 is a direct target of C/EBPα and delays macrophage differentiation

Mol Biol Cell. 2012 May;23(9):1628-35. doi: 10.1091/mbc.E11-05-0412. Epub 2012 Mar 7.

Abstract

Differentiated macrophages are essential for the innate immune system; however, the molecular mechanisms underlying the generation of macrophages remain largely unknown. Here we show that the RNA-binding protein QKI, mainly QKI-5, is transcriptionally activated in the early differentiated monocytic progenitors when CCAAT/enhancer-binding protein (C/EBP) α is expressed. The forced expression of C/EBPα increases the endogenous expression of QKI. Chromatin immunoprecipitation analysis and reporter assays further confirm that C/EBPα activates the transcription of QKI, primarily by binding to the distal C/EBPα-binding site. Blocking the induction of QKI using RNA interference enhances the expression of endogenous CSF1R and facilitates macrophage differentiation. Further study of the mechanism reveals that QKI-5 facilitates the degradation of CSF1R mRNA by interacting with the distal QRE in the 3' untranslated region. In summary, we show that in committed macrophage progenitors, C/EBPα-activated QKI-5 negatively regulates macrophage differentiation by down-regulating CSF1R expression, forming a negative feedback loop during macrophage differentiation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Binding Sites
  • CCAAT-Enhancer-Binding Protein-alpha / genetics
  • CCAAT-Enhancer-Binding Protein-alpha / metabolism*
  • Cell Differentiation / physiology
  • Down-Regulation
  • HL-60 Cells
  • Humans
  • Macrophages / cytology*
  • Macrophages / metabolism
  • RNA-Binding Proteins / genetics
  • RNA-Binding Proteins / metabolism*
  • Receptor, Macrophage Colony-Stimulating Factor / metabolism
  • Transcriptional Activation
  • Tumor Cells, Cultured

Substances

  • CCAAT-Enhancer-Binding Protein-alpha
  • QKI protein, human
  • RNA-Binding Proteins
  • Receptor, Macrophage Colony-Stimulating Factor