mSEL-1L (Suppressor/enhancer Lin12-like) protein levels influence murine neural stem cell self-renewal and lineage commitment

J Biol Chem. 2011 May 27;286(21):18708-19. doi: 10.1074/jbc.M110.210740. Epub 2011 Mar 31.

Abstract

Murine SEL-1L (mSEL-1L) is a key component of the endoplasmic reticulum-associated degradation pathway. It is essential during development as revealed by the multi-organ dysfunction and in uterus lethality occurring in homozygous mSEL-1L-deficient mice. Here we show that mSEL-1L is highly expressed in pluripotent embryonic stem cells and multipotent neural stem cells (NSCs) but silenced in all mature neural derivatives (i.e. astrocytes, oligodendrocytes, and neurons) by mmu-miR-183. NSCs derived from homozygous mSEL-1L-deficient embryos (mSEL-1L(-/-) NSCs) fail to proliferate in vitro, show a drastic reduction of the Notch effector HES-5, and reveal a significant down-modulation of the early neural progenitor markers PAX-6 and OLIG-2, when compared with the wild type (mSEL-1L(+/+) NSCs) counterpart. Furthermore, these cells are almost completely deprived of the neural marker Nestin, display a significant decrease of SOX-2 expression, and rapidly undergo premature astrocytic commitment and apoptosis. The data suggest severe self-renewal defects occurring in these cells probably mediated by misregulation of the Notch signaling. The results reported here denote mSEL-1L as a primitive marker with a possible involvement in the regulation of neural progenitor stemness maintenance and lineage determination.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigens, Differentiation / genetics
  • Antigens, Differentiation / metabolism*
  • Apoptosis / physiology*
  • Astrocytes / cytology
  • Astrocytes / metabolism
  • Basic Helix-Loop-Helix Transcription Factors / genetics
  • Basic Helix-Loop-Helix Transcription Factors / metabolism
  • Cell Line
  • Cell Lineage / physiology*
  • Eye Proteins / genetics
  • Eye Proteins / metabolism
  • Homeodomain Proteins / genetics
  • Homeodomain Proteins / metabolism
  • Intermediate Filament Proteins / genetics
  • Intermediate Filament Proteins / metabolism
  • Intracellular Signaling Peptides and Proteins
  • Mice
  • Mice, Transgenic
  • MicroRNAs / genetics
  • MicroRNAs / metabolism
  • Multipotent Stem Cells / cytology
  • Multipotent Stem Cells / metabolism*
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / metabolism
  • Nestin
  • Neural Stem Cells / cytology
  • Neural Stem Cells / metabolism*
  • Oligodendrocyte Transcription Factor 2
  • PAX6 Transcription Factor
  • Paired Box Transcription Factors / genetics
  • Paired Box Transcription Factors / metabolism
  • Proteins / genetics
  • Proteins / metabolism*
  • Repressor Proteins / genetics
  • Repressor Proteins / metabolism

Substances

  • Antigens, Differentiation
  • Basic Helix-Loop-Helix Transcription Factors
  • Eye Proteins
  • Hes5 protein, mouse
  • Homeodomain Proteins
  • Intermediate Filament Proteins
  • Intracellular Signaling Peptides and Proteins
  • MicroRNAs
  • Mirn183 microRNA, mouse
  • Nerve Tissue Proteins
  • Nes protein, mouse
  • Nestin
  • Olig2 protein, mouse
  • Oligodendrocyte Transcription Factor 2
  • PAX6 Transcription Factor
  • Paired Box Transcription Factors
  • Pax6 protein, mouse
  • Proteins
  • Repressor Proteins
  • Sel1h protein, mouse