Figure 10.

Mechanism of Sox9 function in oligodendrocytes. (a,b) RT–PCR analyses on cDNA obtained from Neuro2A cells transiently transfected with >90% efficiency with expression plasmids for GFP (control) or Sox9. Cells were kept under standard culture conditions (a,–RA in b) or in retinoic-acid-containing medium to induce neuronal differentiation (+RA in b). Transcript levels of glial markers (Fgfr3, GFAP, GlnS, Sox10, CNP, PLP in a), neuronal markers (AMPA receptor, calbindin D₂₈ in b), and a housekeeping gene (actin) were compared semiquantitatively using increasing numbers of amplification cycles (n, n + 3, n + 6). C, water control. (c) Summary of Sox9 function in the p2 and pMN domains of the embryonic spinal cord. Instead of switching from generation of neurons (V2 interneurons and motoneurons, respectively) to glia (astrocytes and oligodendrocytes, respectively), stem cells in both domains continue to primarily produce neurons of the correct subtype. (d) Summary of Sox gene expression in the oligodendrocyte lineage. Sox9 expression precedes the expression of other class E Sox genes, but is no longer expressed in terminally differentiated oligodendrocytes in contrast to Sox10 and Sox8. This pattern of expression explains the observed oligodendrocyte defects in both Sox9- and Sox10-deficient spinal cords.