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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.

New Olig1null mice confirm a non-essential role for Olig1 in oligodendrocyte development