The erbB2 gene is required for the development of terminally differentiated spinal cord oligodendrocytes

We show that erbB2 is not necessary for the early stages of oligodendrocyte precursor development, but is essential for proligodendroblasts to differentiate into galactosylcerebroside-positive oligodendrocytes

Song-Kyu Park


Scholarcy highlights

  • Development of oligodendrocytes capable of forming myelin internodes requires several distinct environmental cues
  • Through a targeted disruption of the murine erbB2 gene, we demonstrate that, in striking contrast to the absence of Neuregulin 1-1, the absence of erbB2 has no effect on the formation of the early oligodendrocyte lineage
  • After transfection and selection of embryonic stem cells, ES cell clones bearing the disrupted erbB2 gene were identified by Southern analysis and injected into C57BL/6 blastocysts
  • Wild-type and erbB2ϩ/Ϫ spinal cord explants develop abundant numbers of differentiated O1ϩ oligodendrocytes, whereas in erbB2Ϫ/Ϫ spinal cord explants, development is halted at the proligodendroblast stage and very few O1ϩ oligodendrocytes develop
  • Neurite and astrocyte development appear normal in erbB2Ϫ/Ϫ explants, myelination is completely absent in erbB2Ϫ/Ϫ explants
  • It seems likely that the lack of differentiated oligodendrocytes in erbB2Ϫ/Ϫ-derived explants reflects cell-intrinsic signaling in OPCs, astrocytes and neurons express NRG receptors and the effects on oligodendrocyte development may result from an erbB2-regulated synthesis of an inhibitor of oligodendrocyte differentiation in these other cell types
  • Viability studies To assess cell death of oligodendrocytes in the presence or absence of erbB2, spinal cord explant cultures were immunolabeled with O4 or O1 mAbs, fixed with 95% ethanol/5% glacial acetic acid for 1 min, incubated with FITC goat anti–mouse IgM, and stained with propidium iodide for 5 min

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