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Publication Detail
New Olig1 null mice confirm a non-essential role for Olig1 in oligodendrocyte development.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Paes de Faria J, Kessaris N, Andrew P, Richardson WD, Li H
  • Publication date:
  • Pagination:
    12, ?
  • Journal:
    BMC Neurosci
  • Volume:
  • Status:
    Published online
  • Country:
  • PII:
  • Language:
  • Keywords:
    Animals, Basic Helix-Loop-Helix Transcription Factors, Brain, Cell Proliferation, Cells, Cultured, Mice, Mice, Knockout, Oligodendroglia, Spinal Cord
BACKGROUND: Olig1 and Olig2, encoding closely related basic helix-loop-helix transcription factors, were originally identified in screens for glial-specific genes. Olig1 and Olig2 are both expressed in restricted parts of the neuroepithelium of the embryonic spinal cord and telencephalon and subsequently in oligodendrocyte lineage cells throughout life. In the spinal cord, Olig2 plays a crucial role in the development of oligodendrocytes and motor neurons, and both cell types are lost from Olig2 null mutant mice. The role of Olig1 has been more cryptic. It was initially reported that Olig1 null mice (with a Cre-Pgk-Neo cassette at the Olig1 locus) have a mild developmental phenotype characterized by a slight delay in oligodendrocyte differentiation. However, a subsequent study of the same line following removal of Pgk-Neo (leaving Olig1-Cre) found severe disruption of oligodendrocyte production, myelination failure and early postnatal lethality. A plausible explanation was proposed, that the highly expressed Pgk-Neo cassette in the original line might have up-regulated the neighbouring Olig2 gene, compensating for loss of Olig1. However, this was not tested, so the importance of Olig1 for oligodendrocyte development has remained unclear. RESULTS: We generated two independent lines of Olig1 null mice. Both lines had a mild phenotype featuring slightly delayed oligodendrocyte differentiation and maturation but no long-term effect. In addition, we found that Olig2 transcripts were not up-regulated in our Olig1 null mice. CONCLUSIONS: Our findings support the original conclusion that Olig1 plays a minor and non-essential role in oligodendrocyte development and have implications for the interpretation of studies based on Olig1 deficient mice (and perhaps Olig1-Cre mice) from different sources.
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