Paracrine control of oligodendrocyte differentiation by SRF-directed neuronal gene expression

Nat Neurosci. 2009 Apr;12(4):418-27. doi: 10.1038/nn.2280. Epub 2009 Mar 8.

Abstract

In neurons, serum response factor (SRF)-directed transcription regulates migration, axon pathfinding and synapse function. We found that forebrain-specific, neuron-restricted SRF ablation in mice elevated oligodendrocyte precursors while inhibiting terminal oligodendrocyte differentiation. Myelin gene and protein expression were downregulated and we observed a lack of oligodendrocytes in mixed neuron/glia and oligodendrocyte-enriched cultures derived from Srf(-/-) mutants. Ultrastructural inspection revealed myelination defects and axonal degeneration in Srf(-/-) mutants. Consistent with our finding that neuronal SRF depletion impaired oligodendrocyte fate in a non-cell autonomous manner, neuron-restricted expression of constitutively active SRF-VP16 affected neighboring oligodendrocyte maturation. Genome-wide transcriptomics identified candidate genes for paracrine regulation of oligodendrocyte development, including connective tissue growth factor (CTGF), whose expression is repressed by SRF. Adenovirus-mediated CTGF expression in vivo revealed that CTGF blocks excessive oligodendrocyte differentiation. In vitro, CTGF-mediated inhibition of oligodendrocyte maturation involved sequestration and thereby counteraction of insulin growth factor 1-stimulated oligodendrocyte differentiation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Newborn
  • Axons / metabolism
  • Axons / ultrastructure
  • Brain / cytology
  • Brain / ultrastructure
  • Cell Differentiation / physiology
  • Cells, Cultured
  • Coculture Techniques / methods
  • Connective Tissue Growth Factor / genetics
  • Embryo, Mammalian
  • Gene Expression / genetics
  • Gene Expression / physiology*
  • Gene Expression Regulation, Developmental / genetics
  • Green Fluorescent Proteins / genetics
  • Humans
  • Insulin-Like Growth Factor I / metabolism
  • Mice
  • Mice, Knockout
  • Myelin Sheath / metabolism
  • Myelin Sheath / ultrastructure
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / metabolism*
  • Neuroglia / physiology
  • Neurons / metabolism*
  • Neurons / ultrastructure
  • Oligodendroglia / metabolism
  • Paracrine Communication / genetics
  • Paracrine Communication / physiology*
  • Serum Response Factor / deficiency
  • Serum Response Factor / metabolism*

Substances

  • CCN2 protein, mouse
  • Nerve Tissue Proteins
  • Serum Response Factor
  • insulin-like growth factor-1, mouse
  • Connective Tissue Growth Factor
  • Green Fluorescent Proteins
  • Insulin-Like Growth Factor I