Ascl1 is required for oligodendrocyte development in the spinal cord

• DOI: 10.1242/dev.015370
• Publication Date: 2008-02-21T01:44:23Z
• Authors: Michiya Sugimori; Motoshi Nagao; Carlos M. Parras; Hiroko Nakatani; Mélanie Lebel; François Guillemot; Masato Nakafuku
• Keywords: OLIG2; SOX10

Development of oligodendrocytes, myelin-forming glia in the central nervous system (CNS), proceeds on a protracted schedule. Specification oligodendrocyte progenitors (OLPs) begins early development, whereas their terminal differentiation occurs at late embryonic and postnatal periods. How these distinct steps are controlled remains unclear. Our previous study demonstrated an important role helix-loop-helix (HLH) transcription factor Ascl1 generation OLPs developing spinal cord. Here, we show that is also involved oligodendrocytes development. Ascl1-/- mutant mice showed deficiency myelin-expressing birth. In vitro culture studies demonstrate induction maintenance co-expression Olig2 Nkx2-2 OLPs, thyroid hormone-responsive myelin proteins impaired mutants. Gain-of-function further collaborates with promoting into vitro. Overexpression Ascl1, alone stimulated specification but combinatorial action or was required for oligodendrocytes. Thus, regulates multiple aspects development