Terminal differentiation of myelin-forming oligodendrocytes depends on the transcription factor Sox10.
By C. Stolt, S. Rehberg, M. Ader, P. Lommes, D. Riethmacher, M. Schachner, U. Bartsch, M. Wegner. Genes & Development, 2002
658 citations recorded by the source corpus.
Sox10 is a high-mobility-group transcriptional regulator in early neural crest. Without Sox10, no glia develop throughout the peripheral nervous system. Here we show that Sox10 is restricted in the central nervous system to myelin-forming oligodendroglia. In Sox10-deficient mice progenitors develop, but terminal differentiation is disrupted. No myelin was generated upon transplantation of Sox10-deficient neural stem cells into wild-type hosts showing the permanent, cell-autonomous nature of the defect. Sox10 directly regulates myelin gene expression in oligodendrocytes, but does not control erbB3 expression as in peripheral glia. Sox10 thus functions in peripheral and central glia at different stages and through different mechanisms.
Subfields: Cancer Research, Developmental Neuroscience
View Paper: https://www.semanticscholar.org/paper/04eca54555b68274afb723970b817ea8cc295cbb
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Citations in the corpus
- Competing waves of oligodendrocytes in the forebrain and postnatal elimination of an embryonic lineage (2005, methodology): “We therefore used an antibody to Sox10, which begins to be expressed in OLPs slightly later than Pdgfra but persists in mature OLs well after Pdgfra is downregulated (ref”
- Why does remyelination fail in multiple sclerosis? (2002, background): “cgi?l=6663">Sox10 has a key role in the terminal differentiation of oligodendrocyte-lineage cell”
- The Sox9 transcription factor determines glial fate choice in the developing spinal cord. (2003, methodology): “Oligodendrocyte progenitor numbers recovered at later stages of development, probably owing to compensatory actions of the related Sox10 and Sox8, both of which overlap with Sox9 in the oligodendrocyte lineage.”